Ultraviolet light can damage DNA, triggering a general transient shutdown of gene transcription . This response has been known for a few decades. However, the molecular mechanism underlying transcription shutdown and recovery upon DNA damage is still largely unknown. Also, in contrast to global transcription repression, some genes are activated by UV light . An investigation of this counter-intuitive behavior implies a surprising gene regulation mechanism . The latest studies have focused on identifying novel factors associated with transcription-related changes after UV-induced DNA damage (Figure 4B) . By using next-generation DNA and RNA sequencing technology, the authors have revealed a global switch in pre-mRNA processing resulting in a preference for the production of transcripts containing alternative last exons which are not normally included in the dominant canonical mRNA isoforms. By combining siRNA-mediated functional screening, ASCC3 stands out as a pivotal regulator of transcription following UV damage. Knocking down the short isoform of ASCC3 transcript (functionally a lncRNA) prevented the cells from recovering normal levels of transcription. In contrast, blocking the long isoform of ASCC3 transcript (encoding a full-length protein) increased transcription levels after UV irradiation . This alternative last exon-derived non-coding RNA produced from a protein-coding gene provides a new source of lncRNAs. Too much exposure to UV radiation is the main cause of skin cancer development. A clearer understanding of UV-induced DNA damage repair is crucial in the prevention of skin cancer.