In preclinical models, the inhibition of FAK has shown the potential to increase the sensitivity of rapamycin-resistant tumors to mTORC1 inhibition, suggesting that targeting FAK signaling could be a feasible and effective strategy to enhance the efficacy of mTORC1 inhibitors in resistant cancers (Cuellar-Vite et al., 2022). This evidence concerns the gene PTK2 and cancer.