As HDAC6 expression is regulated by MK-restricted transcription factors, we can hypothesize that the thrombocytopenia associated to the loss-of-function mutations in RUNX1, FLI1, and GATA1 in human pathologies may be partly explained by a decreased expression of HDAC6, more particularly the abnormalities in DMS and granule development. The gene discussed is FLI1; the disease is Thrombocytopenia.