Huyen et al. (2004) and Ljungman et al. (2017) suggested that DOT1L-mediated H3K79me2 marks, otherwise hidden in chromatin under normal conditions, can modify binding by the tandem tudor domain of the human 53BP1 protein after nearby DSB induction. Similar findings were found in colorectal cancer, where DOT1L-mediated H3K79me is required for chromosome structure maintenance, DNA damage checkpoint, and cell recovery via HR (Ljungman et al., 2017; Wood et al., 2018). The gene discussed is DOT1L; the disease is colorectal cancer.