MacroH2A1.1 has more often than macroH2A1.2 been described as a bona-fide tumor suppressor.[55–58] Interestingly, another study found that macroH2A1 can potentiate silencing, heterochromatin formation, and hypermethylation of the tumor suppressor p16 in CRC, but the work did not distinguish between macroH2A1.1 and macroH2A1.2.[64] These insights highlight the importance of developing tools that distinguish between the individual effects of macroH2A isoforms, particularly the macroH2A1 splice variants–both in terms of variant expression as well as subgenomic localization. The gene discussed is MACROH2A1; the disease is neoplasm.