Current evidence indicates that isoforms mH2A1.1 and mH2A1.2 exhibit transcriptional silencing concordance, while in cancer research, the ambiguous translational regulation of mH2A is cell- and cancer-type specific: in lung cancer, mH2A1.1 functions as an endogenous inhibitor of poly ADP-ribosyl polymerase I (PARP-1), linked to tumor-suppressive roles [13]. Here, PARP1 is linked to lung cancer.