A previous study has reported that GM-CSF could induce resistance to imatinib and nilotinib in chronic myeloid leukemia (CML) via the activation of JAK2/STAT5, but didn’t mention the Immunological role of JAK2/STAT5 pathway in anti-tumor therapy [54]. This evidence concerns the gene STAT5A and chronic myelogenous leukemia, BCR-ABL1 positive.