MEN2B (RET M918T) mice with Cdkn2c knock-out (Cdkn2c−/−) developed MTC at a greatly increased incidence compared to MEN2B (RET M918T) Cdkn2c+/− mice and with a higher proliferation rate, suggesting that Cdkn2c loss increases the risk of MTC and enhances MTC progression, in synergy with the RET oncogene [80]. This evidence concerns the gene CDKN2C and medullary thyroid gland carcinoma.