To address the molecular mechanisms underlying sorafenib-induced inhibition of cell proliferation, cell invasion, and in vivo tumor formation, we first examined the effect of sorafenib on the expression of tumorigenesis-associated signaling proteins (RAF1, ERK, c-MYC, cyclin D2, and AKT) in cultured HHUA-SP and -MP cells. The gene discussed is AKT1; the disease is neoplasm.