Several studies indicated erianin impacted ERK and AKT/mTOR pathways,18–20 and the cross-talk between the RAF-MAPK and AKT/mTOR pathways in the proliferation was noticed through the interaction of CRAF and AKT.29 Mechanism analysis indicated that CRAF protomer activation and enhancement of phospho-AKT partly revealed the resistant mechanism of BRAF inhibitors.30 Usually, BRAF inhibitors induce paradoxical activation of MAPK pathway by reinforcing dimerization of BRAF-CRAF in RAS-driven cancers. This evidence concerns the gene BRAF and cancer.