This may be due to somatic mutations and polymorphisms in the promoter and coding regions as well as indirect actions of epigenetic mechanisms, as in the case of peroxiredoxin (PRDX4) in AML, whose expression coincides with histone 3 (H3K23me3) methylation of its promoter [56,57,58]. Here, PRDX4 is linked to acute myeloid leukemia.