ACh in the tumor microenvironment (TME) promotes tumor proliferation by engaging multiple signaling pathways, including the Wingless‐type MMTV integration site family (Wnt), yes‐associated protein (YAP), mitogen‐activated protein kinase (MAPK), and epidermal growth factor receptor (EGFR)/phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (AKT) pathways in gastric cancer (GC), colorectal cancer (CRC), lung cancer (LC), and non–small‐cell lung cancer (NSCLC; Figure 1A) [15, 16, 17, 18, 19, 20]. This evidence concerns the gene AKT1 and neoplasm.