In this context, the dynamic regulation of BMI1 during DNA double-strand break (DSB) repair and its temporary co-localization with γH2AX foci [36, 37] – potentially required to preserve overall genomic integrity in different types of cancer cells – may imply a need for an interaction with MYSM1 or other deubiquitination enzymes to adapt the mono-ubiquitination status of H2A to re-activate transcription. Here, MYSM1 is linked to cancer.