These findings are consistent with prior work which observed no increase in spontaneous tumor formation in ageing macroH2A DKO mice.[19] Taken together, these data suggest that macroH2A has no significant tumor suppressive function in the intestinal epithelium with respect to adenoma initiation resulting from Apc loss, yet do not rule out the possibility that macroH2A content influences further tumor growth and behavior following establishment. The gene discussed is APC; the disease is neoplasm.