BNIP3L is upregulated during reticulocyte differentiation [11], extensive studies on BNIP3L show that it is required for elimination of mitochondria during reticulocyte differentiation [12–15] and, consistently, fully mature erythrocytes in BNIP3L knockout mice retain mitochondria resulting in dysfunctional erythropoiesis and anemia [13, 16]. The gene discussed is BNIP3L; the disease is anemia (phenotype).