After showing that FAK inhibition or YAP knockdown obviously enhanced cancer cell killing outcomes when combined with KRAS G12C inhibitors treatment, our data from testing with diverse different CDX and PDX models showed that AMG510 treatment as a monotherapy resulted in FAK‐related excessive tumor fibrosis, a frequent cause underlying acquired drug resistance.[17, 18] IN10018 efficiently eliminated the fibrogenesis, and conferred synergistic effects, substantially outperforming the tumor growth inhibition effects of AMG510 monotherapy. The gene discussed is PTK2; the disease is cancer.