To clarify whether paradoxical phosphorylation of AKT and ERK were PDGFRβ-dependent, we further exposed HCC cells to PDGFRβ-targeted siRNA, and found that siRNA targeted knockdown of PDGFRβ resulted in dephosphorylation of AKT and ERK significantly (Fig. 2B). The gene discussed is AKT1; the disease is hepatocellular carcinoma.