Preclinical studies with NSCLC cells selected in vitro for resistance to EGFR inhibitions indicated other potential mechanisms of acquired resistance, such as increased expression of FGF2 and FGFR1, in an autocrine bypass loop [50].Another study has identified an acquired amplification of the adaptor protein CRKL (that has known oncogenic properties) in an NSCLC patient that developed resistance to erlotinib [51]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.