Heme-induced Bach1 degradation also promotes the transcription factor SPI-C expression in monocytes and the development of bone marrow macrophages [65], and when Bach1 was overexpressed (under the control of the GATA-1 promoter) in transgenic mice, megakaryocyte maturation was significantly impaired and the animals developed thrombocytopenia, likely because Bach1 suppressed the expression of p45-targeted genes such as thromboxane synthase [66]. The gene discussed is BACH1; the disease is Thrombocytopenia.