Studies in experimental models have shown that HDAC inhibition decreases AML cell proliferation through cell cycle arrest; decreases expression of the stem cell marker CD117; increases mRNA levels of hematopoietic transcription factors involved in differentiation; increases expression of the myeloid differentiation marker CD11b/CD18 (integrin αMβ2) and causes morphological signs of neutrophil/monocytic differentiation (i.e., reduced nuclear:cytoplasmic ratio, condensation of nuclear chromatin together with infrequent detection of the nucleolus and increased azurophilic granulation) [172]. Here, KIT is linked to acute myeloid leukemia.