Bnip3L null mice develop anemia and thrombocytosis due to mitochondrial retention in erythrocytes, impairing erythroid maturation and increasing platelet number by preventing Bnip3L-mediated autophagic degradation of mitochondrial protein Bcl-XL, which inhibits the activation of mitochondria-mediated apoptosis. This evidence concerns the gene BNIP3L and thrombocytosis disease.