These included clinically relevant associations between alterations in BRAF, ERBB2, EGFR, and the BCR-ABL fusion gene and sensitivity to clinically approved drugs in defined tumor types, as well as associations between KRAS, PDGFR, PIK3CA, PTEN, CDKN2A, NRAS, TP53, and FLT3 with drugs that target their respective protein products or pathways (Figure 4B; Table S4C). This evidence concerns the gene TP53 and neoplasm.