Dr. Alexandra Nusawardhana, the lead author of the study and who earned her doctorate in biomedical sciences this year from Penn State College of Medicine, conducts research to understand genomic instability and cancer treatment response.
Credit: Jason Plotkin / Penn State. Creative Commons
A characteristic of evolved biological systems, and one that distinguishes them from systems designed from first principles, is that they are often unnecessarily complex, vulnerable to failure and dependent on layers of patchwork compensation. This is what we should expect from systems produced by utilitarian, suboptimal compromises built from whatever was available at the time.
With no plan, no foresight and no predetermined objective, natural selection can only favour whatever leaves more descendants in a particular environment. The result is not an ideal solution, but merely a workable one — one that is better than what preceded it, even if it remains a very long way from perfection. An intelligent designer, such as the one proposed by advocates of intelligent design, would be under no such historical constraints and could, in principle, rebuild a system from scratch to arrive at the optimal solution.
To illustrate this, this post and the next will look at two recent papers that incidentally demonstrate how many human health problems arise from these over-complex, error-prone systems — systems that would not exist if the human body were the pinnacle of created perfection that creationists imagine it to be. Unless, of course, the designer intended us to suffer when its systems failed.
The first concerns a paper published in February 2026 in Nature Communications by researchers at Penn State College of Medicine. It shows how one component of the DNA repair machinery — a system needed because DNA replication and maintenance are themselves vulnerable to error and damage — can itself go wrong and produce a pattern of genomic instability resembling that seen when the BRCA1 and BRCA2 tumour-suppressor pathway is defective.
The culprit is EXO1, a gene that encodes an exonuclease involved in DNA processing and repair. In normal cells, EXO1 helps trim and process damaged or mismatched DNA so that repair can proceed. But when EXO1 is overexpressed, as the researchers found in a significant proportion of several cancers, including about 20–30% of breast and ovarian cancers as well as melanoma, testicular, cervical and hepatobiliary cancers, too much of this normally useful protein becomes destructive. Instead of helping to preserve genome integrity, excessive EXO1 activity can degrade newly synthesised DNA during replication stress, expanding single-stranded DNA gaps and degrading reversed replication forks.
The result is a BRCA-like pattern of genomic instability even in cells whose BRCA pathway is still functional. In other words, the cell behaves in some important respects like a BRCA-mutant tumour cell, not because BRCA1 or BRCA2 is mutated, but because too much EXO1 has overwhelmed the normal protective system. This matters clinically because such tumours may respond to some of the same treatments used against BRCA-mutant cancers, including drugs that target DNA repair vulnerabilities.
So, we have a DNA replication and maintenance system that needs elaborate repair machinery because the genome is constantly vulnerable to damage; then we have the catastrophic consequences when that repair machinery itself goes rogue. Compare that with the simpler, more robust system we might expect from an intelligent designer endowed with foresight and unconstrained by evolutionary history. Complexity is not the hallmark of intelligent design that creationists claim it to be. In biology, it is very often the accumulated consequence of failure-prone, suboptimal compromises produced by evolutionary tinkering without a predetermined objective.

































