Colon malignancies overexpress the CHRM3 gene and protein, and post-mAChR M3 signaling promotes cell proliferation; the interplay between EGFR/ERK and protein kinase C (PKC)/p38 mitogen-activated protein (MAP) kinase signaling pathways is complex after mAChR M3 signaling; then, the formation of an invasive and metastatic phenotype requires these signaling interactions to increase the cellular release of MMP1; hence, targeting mAChR M3, post-mAChR M3 signaling, or MMP1 to prevent or reverse colon cancer invasiveness offers therapeutic potential [136]. This evidence concerns the gene EGFR and colonic neoplasm.