In colon cancer cells treated with the deacetylase inhibitor sulforaphane (SFN) [23–26], acetylation of CCAR2 in the C-terminus established an acetyl ‘switch’ site [27], whereas acetylation in the N-terminus provided recognition motifs for the bromodomains of BAZ1A and ASH1-like protein (ASH1L). This evidence concerns the gene ASH1L and colonic neoplasm.