To further verify the function of ATG4B in leukemia progression in vivo, 2 × 105 MLLT3‐KMT2A‐overexpressing mouse AML cells were transplanted into recipient mice (hereafter referred to as AML model mice) and treated with or without the ATG4B inhibitor tioconazole.[17] The survival of AML model mice was assessed. The gene discussed is ATG4B; the disease is acute myeloid leukemia.