Increased PI3K/AKT/mTOR signaling, independent of changes in upstream receptor tyrosine kinases has been described in DMS114 lung cancer cells (FGFR1 amplified) and RT112 urothelial cancer cells (FGFR3-TACC3) following chronic treatment with infigratinib[56]. This evidence concerns the gene FGFR1 and lung carcinoma.