Upon UV irradiation, p53 activation, mediated by DNA-PK (DNA-dependent protein kinase) and ATM (ataxia telangiectasia mutated), arrests cells in G1/S, intra S, and G2/M phases through up-regulation of p21Cip1 and the subsequent inhibition of CDK (cyclin-dependent kinase)-cyclin complexes and PCNA (proliferating cell nuclear antigen) [41,42,43]. The gene discussed is PCNA; the disease is telangiectasis.