The administration of FGF8, FGF17, or FGF18 could resist apoptosis and enhance the survival of serum-starved tumor cells, including HCC-1.2, HepG2, and Hep3B cells, the mechanism studies have found that these effects were mediated by ERK and AKT/mTOR signaling pathways (Gauglhofer et al., 2011; Liu et al., 2015a). Here, AKT1 is linked to neoplasm.