We also identified altered p16-CDK4/6-RB activity as a likely cooperative event for CRTC1-MAML2–induced tumorigenesis in vivo and showed that a combination of EGFR and CDK4/6 inhibition effectively blocked MEC, thus revealing a potential effective treatment for patients with MEC. The gene discussed is MAML2; the disease is mucoepidermoid carcinoma.