During mouse lens development, the expression of p53/Mdm2 was spatiotemporally regulated.24 Loss of p53 activity through expression of viral genes or the endogenous gene knockout induces posterior subcapsular cataracts.21, 47, 48 Besides, overexpressing human p53 in mouse lens led to microphthalmia.22 At the molecular level, p53 has been shown to regulate both major lens transcription factors c-Maf, Prox-126 and differentiation-related crystalline genes.49, 50 In addition, p53 regulates numerous apoptotic genes, some of which are implicated in regulating lens differentiation. Here, TP53 is linked to microphthalmia.