DDX5 and osteosarcoma: Specifically, the authors reported that (i) DDX5-deficient human osteosarcoma U2OS cells exhibited asymmetric end deletions on the side of the DSBs with significant overlap with a transcribed gene; (ii) DDX5 bound RNA transcripts near DSBs; (iii) DDX5 was excluded from DSBs in a transcription- and ATM activation-dependent manner; (iv) DDX5-deficient cells had increased R-loops near DSBs leading to delayed exonuclease 1 and replication protein A (RPA) recruitment to laser irradiation-induced DNA damage sites, resulting in homologous recombination repair defects [30].