CDKN2A and nasopharyngeal carcinoma: We generated primary and orthotopic NPC models starting from normal nasopharyngeal epithelium with NPC related genetic drivers, a capable strategy that we have successfully applied for lung cancer,[21] gastric cancer,[22] bladder cancer,[23] and others.[24] With these models, we further investigated the biological functions of multiple important genetic alterations, including Trp53, Cdkn2a, and Tgfbr2 loss and LMP1 overexpression, during NPC initiation and development.