Treatment resistance associated with FGFR gene family member alterations is the result of activation of downstream intracellular signaling pathways, including the RAS/MAPK pathway, the most common pathway associated with FGFR-mediated treatment resistance[57,68], and the PI3K/AKT/mTOR pathway, which has previously been identified as playing a key role in FGFR-dependent tumor progression and treatment resistance[69-71]. Here, AKT1 is linked to neoplasm.