Intriguingly, although Ascl2 can increase the number of ISCs and its expression is positively correlated with CRC progression [114], forced expression of Ascl2 in a mouse model of colon cancer doesn’t accelerate tumourigenesis, which suggests ectopic expression in cells that do not normally express Ascl2, rather than overexpression, explain the aetiology of Ascl2 in CRC [115]. Here, ASCL2 is linked to colorectal carcinoma.