Nonetheless, previous studies proposed that acetate inhibits proliferation and induces apoptosis in colon cancer cells3, 4, 5, 6 and that acetate-induced apoptosis in CRC cells involves different biochemical events, including mitochondrial alterations.3, 4, 5 We have also previously shown that acetate induces apoptosis in CRC-derived cells in a dose-dependent manner, characterized by DNA fragmentation, caspase-3 activation, phosphatidylserine exposure to the outer leaflet of the plasma membrane and the appearance of a sub-G1 population5. The gene discussed is CASP3; the disease is colorectal carcinoma.