Nitulescu et al. experimentally demonstrated that STAT1 activates the JAK-STAT pathway through phosphorylation at Ser727 to promote AML growth and malignant biological behaviors [41], whereas Gao et al. mediated the phosphorylation of the 727 site using diptoindonesin G to promote AML cell differentiation through the ERK pathway [42]. Here, STAT1 is linked to acute myeloid leukemia.