AKT1 and neoplasm: Yang et al. (2010) also revealed that SNPE significantly reduced the viability of HepG2 cells (IC50 = 0.86 mg/ml). The mechanism of action study showed that SNPE inhibited TPA-induced HepG2 migration and invasion via blocking the expression of PKCα and attenuated p38 and p38/ERK activation (Yang et al., 2010). Moreover, SNPE inhibited the viability of HepG2 cells through the suppression of the VEGF-induced activation of AKT and mTOR in vitro and reduced the volume and weight of the tumors in the HepG2 tumor-bearing mouse model (Yang et al., 2016).