Because FAK activity is implicated in KRAS-driven tumor biology and in stromal resistance mechanisms, the combination of a MAPK pathway clamp (avutometinib) with FAK inhibition (defactinib) was developed to specifically target both tumor-intrinsic signaling and pro-tumor stromal support, respectively (McNamara et al., 2024[80]). This evidence concerns the gene PTK2 and neoplasm.