This could be explained by the rapid development of leukemia we observed in ATG7+/+ compared to ATG7−/− mice; due to the differentiation of LT-HSCs following BCR-ABL expression previously reported in this model [38], a more advanced stage of disease in the autophagy competent mice would mask the decrease of LT-HSCs following ATG7 deletion. The gene discussed is ATG7; the disease is leukemia.