TP53 and Mobius syndrome: Moreover, DNA‐PKcs‐dependent p53 activation was key inhibitor of MB tumorigenesis in Ptch1+/− mice, because mice with disruption of other NHEJ core components such as DNA Ligase 4 (Lig4), X‐ray repair cross‐complementing protein 4 (XRCC4), Ku80 and Artemis developed MBs only in p53‐null experiments, signifying a stern dependence of tumorigenesis on the blockade of p53 surveillance mechanisms.61, 62