This work though notes that mice with a heterozygous CHK1 gene knockout are phenotypically normal, with no signs of anemia within their first year of life.[9] Moreover, the CHK1 inhibitor GDC‐0575 kills acute myeloid leukemia (AML) cells in mice when combined with the nucleoside analogue cytarabine and the cytokine G‐CSF, which mobilized hematopoietic stem cells.[13] Therefore, an optimal CHK1 inhibitor should be only active against the activated CHK1 in chemotherapy‐treated tumor cells, but not the inactive CHK1. This evidence concerns the gene CSF3 and acute myeloid leukemia.