As shown for BCR-ABL1, mutations in the binding domain of a respective kinase inhibitor or its overexpression/gene amplification have been observed in multiple tumors leading to drug resistance, as shown for acquired EGFR T790M mutations and c-MET receptor tyrosine kinase amplification promoting gefitinib resistance in lung cancer or KIT exon 14 or 17 and PDGFRA exon 14 mutations providing resistance against imatinib and reduced efficacy of sunitinib in GIST (Lynch et al., 2004; Gao et al., 2013; Kobayashi et al., 2013; Zhang et al., 2019). The gene discussed is EGFR; the disease is lung cancer.