Sessa et al. [35] report that (i) the tumor suppressor BRCA2 protein physically interacts with DDX5 in cancer cells (Fig. 2D); (ii) DDX5 depletion leads to a genome-wide accumulation of DNA-RNA hybrids particularly enriched at the DSB sites, which can be rescued by DDX5 overexpression in both DDX5-depleted cells and BRCA2-depleted cells [35]; (iii) BRCA2 helps retain DDX5 on DNA damage sites and stimulates R-loop-unwinding activity of DDX5; and (iv) DDX5-BRCA2 interaction favors DNA DSB repair by homologous recombination (HR) [35]. The gene discussed is DDX5; the disease is cancer.