The common mechanism by which procaine inhibited cancer cell proliferation and migration was the inactivation of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK)/focal nuclear adhesion kinase (FAK) and protein kinase B (AKT)/extracellular signal-regulated kinase (ERK) pathways [134, 135]. The gene discussed is AKT1; the disease is cancer.