However, other chromatin readers depend on specific histone methylations to be recruited to DNA damage sites, such as 53BP1 (Pei et al., 2011; Wakeman et al., 2012; Zhao et al., 2020), a protein involved in non-homologous end joining (NHEJ) (Lottersberger et al., 2013; Panier and Boulton, 2014; Shibata, 2017), a key DNA repair pathway in resting cells such as neurons or cancer stem cells. This evidence concerns the gene TP53BP1 and cancer.