Insilico Medicine published preclinical data showing an AI‑designed proteolysis‑targeting chimera (PROTAC), D16‑M1P2, selectively degrades PKMYT1 and produced anti‑tumor activity in cell lines and xenograft models with CCNE1 amplification or FBXW7/PPP2R1A alterations. The work appeared in Nature Communications and describes Chemistry42 generative models enabling linker and ligand optimization for a bifunctional degrader. The program exemplifies AI’s maturation in therapeutic design, producing a preclinical lead with biomarker‑driven patient selection rationale. Insilico’s approach prioritizes genomic contexts where synthetic‑lethality dependence is strongest, suggesting future clinical plans will target genomically defined cohorts rather than single histologies—an execution path that could accelerate first‑in‑human studies if translational biomarkers validate.