Comment by epistasis

Yes, and one of the hallmarks of cancer is a removal of the usual DNA damage checkpoints. Cells have sensors that detect damaged DNA and stop cell division, and once that is gone evolution happens on an extremely accelerated times scale. In lung cancer, for example, we have developed entire series of drugs to go after successive resistance mutations inside the EGFR gene.

When we first started getting good at sequencing the DNA of tumors, I remember initial reports of taking samples across the 3D space of a tumor and finding great spatial heterogeneity in the tumor genomes.

I'm actually most excited for using this drug in combination with colon cancer, where KRAS mutation is a common drug resistance evolution in response to drugs that target the gene EFGR (though cancer researchers may all have their favorites to go after, colon cancer went after my family especially hard).