It has been postulated that mitophagy contributes to differentiation and development by participating to the intracellular remodelling that occurs for example during haematopoiesis and adipogenesis. In mammalian red blood cells, the expulsion of the nucleus followed by the removal of other organelles, such as mitochondria, are necessary differentiation steps. Nix/Bnip3L, an autophagy receptor whose structure resembles that of Atg32, is also an outer mitochondrial membrane protein that interacts with GABARAP [170, 171] and plays an important role in mitophagy during erythroid differentiation [172, 173] (Figure 3(c) ). Although autophagosome formation probably still occurs in Nix/Bnip3L deficient reticulocytes, mitochondrial elimination is severely impaired. Consequently, mutant reticulocytes are exposed to increased levels of ROS and die, and Nix/Bnip3L knockout mice suffer severe anemia. Depolarization of the mitochondrial membrane potential of mutant reticulocytes by treatment with an uncoupling agent results in restoration of mitophagy [172] , emphasizing the importance of Nix/Binp3L for the mitochondrial depolarization and implying that mitophagy targets uncoupled mitochondria. Haematopoietic-specific Atg7 knockout mice also exhibited severe anaemia as well as lymphopenia, and the mutant erythrocytes markedly accumulated degenerated mitochondria but not other organelles [174] . The mitochondrial content is regulated during the development of the T cells as well; that is, the high mitochondrial content in thymocytes is shifted to a low mitochondrial content in mature T cells. Atg5 or Atg7 deleted T cells fail to reduce their mitochondrial content resulting in increased ROS production as well as an imbalance in pro-and antiapoptotic protein expression [175] [176] [177] . All together, these evidences demonstrate the essential role of mitophagy in haematopoiesis.