Furthermore, knockdown of phosphoinositide-dependent kinase-1 by siRNA, which com pletely blocked the CHKA-mediated AKT (T hr308) activation, also didn’t affect CHKA-triggered AKT (Ser473) phosphorylation and HCC cell metastatic phenotype (Supplementary Figure 8), suggesting that neither phosphoinositide-dependent kinase-1 nor AKT (T h r308) activation has an essential function in CHKA-induced HCC metastasis. Oddly enough, siRNA-mediated knockdown…