Silencing of ACSS2 in cancer cells reduces incorporation of acetyl unit from acetate into either lipids or histones more than suppression of ACSS1 or ACSS3. ACSS2 is highly expressed in several human tumors, and loss of ACSS2 suppresses tumor development in a mouse cancer model of cMyc combined with PTEN knockout [48]. This evidence concerns the gene MYC and neoplasm.