Notably, UV radiation – another activator of ssRNA breaks, ATR and Chk1 – has also been described to induce N-SMase activity, and tumor resistance to apoptosis by UV has been linked to failure of N-SMase activation.45, 46 Although the specific NSMase as well as its regulation had not been studied, our study suggests that nSMase2 could be the isoform also responsible for NSMase activity increase in response to UV. This evidence concerns the gene SMPD3 and neoplasm.