Cancer tends to evolve at a rate that outpaces treatment innovation, and the molecular determinants can be wildly heterogenous. For example, a lung cancer patient can have half a dozen tumors that all harbor independent oncogenic drivers. It is not uncommon for a patient to undergo treatment with a target therapy and see complete tumor responses in some lesions, while others grow unimpeded.
We did not develop our own code base. Humans are a black box and drug development is HARD.
Btw, there is still research that tries to find a general mechanism for interventions. The other day I looked at interesting work that hinged the delivery of disruptive payload on telomerase activity. Telomerase is expressed almost universally in cancer cells and in stem cells; therefore somatic cells would be spared, and it’s hoped that stem cells would be able to recover.
Anyway like you said, both approaches are meaningful, which is why it’s important to tell them apart.