A number of different compensatory mechanisms to selective FGFR inhibitors in the preclinical setting have been described in cell lines harbouring FGFR1 amplification, such as the activation of the PI3K/AKT pathway upon FGFR inhibition with infigratinib in a SCLC cell line [125], and the activation of the JAK-STAT pathway in a NSCLC cell line chronically exposed to AZD4547 or infigratinib [126]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.