Therefore, the data from both human MEC xenografts and GEMM-derived MEC allografts indicate that the combined inhibition of the CRTC1-MAML2 fusion–induced EGFR signaling and the secondary, altered pathway p16-CDK4/6-Rb signaling effectively blocks MEC in these preclinical MEC models. Here, CDKN2A is linked to mucoepidermoid carcinoma.