BRAF and neoplasm: In a recent study, a retrospective analysis of 17 iCCA patients receiving FGFR inhibitors, such as Pemigatinib and Futibatinib, revealed that nearly 50% developed secondary mutations in MAPK-related genes, such as KRAS and BRAF, leading to the hyperactivation of the MAPK pathway, which compromised the inhibitory drug, encouraging tumor growth [145].