Preclinical study showed that the reactivation of RAF-MEK-ERK signaling was observed in NTRK1-driven pancreatic cancer and lung cancer treated with entrectinib, which was possibly one of the acquired-resistance mechanisms to entrectinib, and combined inhibition of TRKA plus MEK1/2 markedly forestalled the onset of drug resistance in both models (85). This evidence concerns the gene NTRK1 and lung carcinoma.