It is important to underline that many recurrent mutations in MDS are involved in the regulation of oxidative status in MDS microenvironment: for example, TET2 recruited histone deacetylase enzyme 2 (HDAc2) and repressed transcription of interleukin-6 (IL-6), one of the most important inflammation cytokines that promotes inflammation and ROS production [22, 23]; ASXL1 mutation causes ROS increase via NAD(P)H oxidase and consequent cell death by pyroptosis [24]. Here, HDAC2 is linked to myelodysplastic syndrome.