Mechanistically, CM-248aa competitively targets the acidic domain of SET nuclear oncogene (SET), endogenously inhibiting the SET–protein phosphatase 2A interaction to promote the dephosphorylation of AKT, extracellular signal-regulated kinase, and p65, which ultimately inhibits the proliferation and metastasis of GC cells [46]. The gene discussed is AKT1; the disease is gastric cancer.