Junk DNA Can Fight Cancer

Scientists now declare that parts
of human DNA formerly thought of
as “junk” have anti-cancer properties

From Junk to Genius
Junk DNA Now Found to Fight Cancer

by Dr. Sarah Buckland-Reynolds

In a stunning reversal of scientific dogma, Zeisig and other researchers at King’s College London have discovered that so-called “junk DNA”, long dismissed as evolutionary leftovers, can be weaponized against cancer.

Their study, published in the journal Blood in October 2025, reveals that transposable elements (TEs), once considered genomic clutter, become hyperactive in certain blood cancers and create vulnerabilities that existing cancer drugs can exploit. But beyond its therapeutic promise, this discovery shakes the foundations of evolutionary theory, reframes assumptions about genomic architecture, and points toward intelligent design.

Challenging Erroneous Evolutionary Assumptions

For decades, evolutionary biology has taught that vast stretches of the human genome are non-functional, presumed to be meaningless vestiges from failed mutations carried down from our evolutionary ancestors. These repetitive sequences, known as transposable elements (TEs), make up about 45-50% of our DNA. They were labeled “junk” because they did not code for proteins, and were therefore assumed to serve no purpose. This assumption is consistent with the materialist framework that Darwinian evolution depends on – as it assumes that biological systems and processes are built through trial and error.

Over time, however, scientists began discovering roles for these genomic regions in gene regulation, genome stability, and cellular defense within what they had once labeled as “junk.” This new discovery by King’s College not only adds to the growing evidence of functionality in previously dismissed regions of human DNA but also further challenges long-held evolutionary assumptions.

A profound contribution of the King’s College discovery is the finding that these sections of the human genome become functional under certain conditions. In the words of the authors: “TEs… historically regarded as ancient junk sequences… are tightly regulated by epigenetic and transcription factors.” More specifically, they found that when key regulatory genes (ASXL1 and EZH2) are mutated, TEs become abnormally active, triggering DNA damage in cancer cells. This stress creates a therapeutic window: by using existing cancer drugs (PARP inhibitors) to block DNA repair, researchers caused the cancer cells to collapse.

Form Does Not Always Precede Function

This finding of a latent function that activates under certain conditions challenges a central assumption of evolutionary genomics regarding evolutionary biology: that function emerges from form. The discovery that “junk DNA” has critical regulatory and therapeutic functions (as seen in the King’s College cancer study) undermines the assumption that lack of apparent form (e.g., no protein-coding role or conservation) implies lack of function. This shift therefore should prompt a reevaluation of how function is inferred in genomics.

The study further elaborated on the surprising activation of DNA Repair Pathways in ERV expressing cells not predicted by evolutionary models. In the words of the authors:

“Interestingly, we also observed activation of multiple DNA damage repair (DDR) pathways in these cells, indicating excessive DNA damage, an established feature for reactivation of TEs.”

The authors’ experiments showed that these pathways were not randomly triggered; rather, they respond specifically to TE reactivation.

A Better Framework for Explanation

Evolutionary theory struggles to explain how such precise, context-dependent responses could arise from random mutation and selection. The coordination between TE activity and DNA repair implies foresight. While these findings expose flawed assumptions in evolutionary theory, these observed context-dependent, latent functionalities are consistent under a design-based framework.

Moreover, the study shows that TEs can influence cell fate without producing proteins. This challenges the protein-centric view of evolution. The point emerges that: If non-coding sequences can drive biological outcomes, then the genome is far more complex than previously thought. Evolutionary models, which rely on gradual changes in coding regions, are ill-equipped to account for this complexity.

Genomic Assumptions: A Recalibration Required

The conditional activation of TEs also has implications for genomic dating and evolutionary timelines. Transposable elements (TEs) often serve as molecular clocks, helping scientists estimate the age of genetic sequences and the timing of evolutionary divergence by examining mutation rates, sequence conservation, and patterns across species. These methods rely on the assumption that TEs are ancient, inactive remnants. However, as Zeisig et al’s study shows, many TEs are not inert, but may be reactivated under certain conditions and regulated. This undermines the idea that they are passive markers of time.

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These findings further challenge assumptions underlying genomic dating, including the notions of constant mutation rates and neutral evolution—assumptions that may not hold in dynamic or stress-responsive regions such as transposable elements (TEs). These findings therefore suggest that the activity of TEs may reflect environmental conditions, mutational stress, or epigenetic regulation more accurately than genetic age. This calls into question the reliability of TE-based dating models and the broader use of molecular clocks.

In addition to this, the study shows that TE activity can be modulated by reverse transcriptase inhibitors (drugs that block their replication). This suggests that TE dynamics are not fixed but may be externally tunable. This therefore opens further uncertainty because it raises the possibility that past TE activity may have been influenced by factors that are beyond reconstruction.

A New Paradigm for Cancer and Creation, and a Call to Praise

In addition to exposing evolutionary assumptions, the implications of the King’s study are encouraging, as they expose a pathway already existing within our bodies’ engineering to unlock new treatments for cancers that lack protein-based drug targets. As Professor Chi Wai Eric of King’s College stated in a ScienceDaily commentary on the study:

“This discovery offers new hope for patients with hard-to-treat cancers… turning what was once thought to be useless DNA into a powerful target for treatment.”

For a portion of our DNA once dismissed as functionless (a vestige of an evolutionary past marked by decay) this study brings science full circle, revealing that the very elements once deemed random may in fact hold pathways to regeneration and health. This striking contrast—where remnants once thought to be “junk” are now recognized as life-enabling—exposes the limitations of evolutionary thinking. By dismissing much of the genome as junk, scientists may have overlooked powerful tools for healing and understanding. The rediscovery of TE functionality is a humbling reminder that design often hides in plain sight.

As science continues to uncover the hidden layers of the genome, the case for intelligent design grows stronger. It has now become even clearer that our genome is not a patchwork of accidents; rather, it is a tapestry of intention. For believers in creation, the activation of so-called “junk” DNA under stress is no surprise; it stands as a testament to divine foresight. For skeptics, it poses a challenge to rethink the assumptions that have guided genomic research for decades.

In the end, the King’s College study does more than offer a new cancer therapy: it invites us to reconsider the nature of life itself, not as a product of chance, but as a reflection of purpose. As the Bible puts it in Psalm 139:13–14 (NIV): “For you created my inmost being; you knit me together in my mother’s womb. I praise you because I am fearfully and wonderfully made; your works are wonderful, I know that full well.”

Dr. Sarah Buckland-Reynolds is a Christian, Jamaican, Environmental Science researcher, and journal associate editor. She holds the degree of Doctor of Philosophy in Geography from the University of the West Indies (UWI), Mona with high commendation, and a postgraduate specialization in Geomatics at the Universidad del Valle, Cali, Colombia. The quality of her research activity in Environmental Science has been recognized by various awards including the 2024 Editor’s Award from the American Meteorological Society for her reviewing service in the Weather, Climate and Society Journal, the 2023 L’Oreal/UNESCO Women in Science Caribbean Award, the 2023 ICETEX International Experts Exchange Award for study in Colombia. and with her PhD research in drought management also being shortlisted in the top 10 globally for the 2023 Allianz Climate Risk Award by Munich Re Insurance, Germany. Motivated by her faith in God and zeal to positively influence society, Dr. Buckland-Reynolds is also the founder and Principal Director of Chosen to G.L.O.W. Ministries, a Jamaican charitable organization which seeks to amplify the Christian voice in the public sphere and equip more youths to know how to defend their faith.