FAK signaling has been reported to regulate fibrogenesis within tumors,[17, 48] and excessive fibrosis is correlated with drug resistance, because it can create a barrier that prevents interactions between cancer cells and therapeutic agents.[49] In the present study, AMG510 treatment of three models (1 NSCLC CDX (NCI‐H2122), 1 CRC PDX (CO‐04‐0070), and 1 NSCLC PDX (LU‐01‐0030)) resulted in excessive fibrogenesis, and this was accompanied in each case by hyperactivated FAK signaling. This evidence concerns the gene PTK2 and non-small cell lung carcinoma.