In addition, DNMT3A-R882H significantly accelerated the progression of leukemia in the presence of other known mutations, such as NRAS-G12D, NPM1c, or IDH1R132H coexisting with the DNMT3A mutation in human AMLs, providing a susceptible genetic background in epigenetically misregulating the expression of HOX genes [87]. The gene discussed is DNMT3A; the disease is leukemia.