We investigated whether the causal genes are enriched in CMSs of CRC: CMS1 (MSI immune): tumors with high microsatellite instability (MSI-H) and strong immune activation; CMS2 (canonical): tumors with features of traditional CRC, characterized by WNT and MYC signaling activation; CMS3 (metabolic): tumors with metabolic dysregulation and KRAS mutations; CMS4 (mesenchymal): tumors with prominent stromal infiltration, inflammation, and angiogenesis [2]. This evidence concerns the gene KRAS and colorectal carcinoma.