In different models of solid and hematopoietic tumors, the use of selective HDACi targeting class I HDAC (mocetinostat, entinostat, and romidepsin) as single agent elicited beneficial effects on different antitumor effectors, increasing T lymphocyte infiltration or upregulation of MICA/MICB on the tumor cell surface, thus enhancing natural killer (NK) cell activity through an increase in the ligation of the activating receptor NKG2D, which interacts with MICA and MICB [35,36,37,38] (Table 1). The gene discussed is MICA; the disease is neoplasm.