As defective lymphopoiesis of Mysm1-deficient mice could be rescued almost completely by deletion of p53, and also other anomalies – including growth retardation, neurological deficit, and skin atrophy – were ameliorated in p53−/−Mysm1−/− DKO mice, interplay of Mysm1 and p53 appears to be a common principle in several sequential differentiation processes. Here, TP53 is linked to skin atrophy.