In line with previous reports showing that the CXCL10/CXCR3 axis activates MEK and ERK signaling in several cancer types,42–44 our results demonstrated that ERK signaling was modulated by TKI-induced expression of CXCR3, which could be abrogated by GSI or CXCR3-specific inhibitors in FLT3/ITD + AML cells. This evidence concerns the gene CXCL10 and acute myeloid leukemia.