Further categorization of CRC according to these 3 genomic alterations revealed a significantly higher rate of dMMR/BRAF+APC- in late-onset CRC (18% vs. 2.0% in traditional-onset CRC), supporting MLH1 promoter hypermutation driven by BRAF p.V600E as the predominant mechanism of the increased rate of dMMR disease in late-onset CRC. Here, APC is linked to colorectal carcinoma.