Given that UVR primarily induces DSBs [13], the aims of this study were to investigate the expression of ATM and activated ATM (pATM) in both normal skin as well as in the spectrum of premalignant actinic keratosis (AK) to carcinoma in-situ (CIS) to invasive SCC lesions, to see whether the model proposed by Bartkova et al. could be extended to include cutaneous SCCs. The gene discussed is ATM; the disease is in situ carcinoma.