Colorectal carcinogenesis and progression occur through a multi-step process, most often starting from an adenoma that has the potential to progress to carcinoma through deregulation of Wnt/β-catenin/adenomatous polyposis coli (APC) signaling with subsequent accumulation of epigenetic alterations and somatic mutations and driven by interactions with the metabolic and immune status of the tissue microenvironment (TME) [12,14,26]. Here, APC is linked to carcinoma.