Indeed, H3.3 gliomas tend to co-mutate DNA repair enzymes that also have a role in 53BP1 nuclear body formation, which could suggest that bypass of the 53BP1 response is favorable for H3.3K27M (tumor) cells as disruption of such a repair mechanism might prevent resolving the DNA damage resulting from UFBs and thus enhance genome plasticity and heterogeneity of the tumor, and ultimately help the cancer cells to thrive [4]. The gene discussed is TP53BP1; the disease is cancer.