ASCL2 and colorectal carcinoma: Consistently, a genome-scale CRISPR screen using an endogenous WNT reporter identified KMT2A as a regulator of canonical β-catenin transcriptional activity, and the loss of KMT2A by CRISPR-mediated knockout led to induction of KRT20 and suppression of intestinal stem cell markers (LGR5 and ASCL2) in CRC cells19.