Our suspicion is based on: (1) knowledge that the genomic regions marking the boundaries of somatic CNVs found in many cancers tend to be replicated at the same time and share a long-range interaction (De and Michor, 2011); (2) reports that Rad52 promotes DSB repair by MMEJ in fission yeast, and during antibody class-switch recombination in mouse B cells (Decottignies, 2007; Zan et al., 2017), albeit the same may not be true in budding yeast (Meyer et al., 2015). Here, RAD52 is linked to cancer.