Because the treatment of human cancer cells with HDAC inhibitors consistently leads to up-regulation of p21 expression, a cyclin-dependent kinase inhibitor that is a well-established target of HDAC inhibitors [6], [7], [12], we sought to determine whether overexpression or knockdown of HDAC4 could affect p21 regulation and to speculate the mechanism of HDAC4-mediated growth promotion in gastric cancer cells. The gene discussed is HDAC4; the disease is cancer.