Overall, these findings are supported by recent work in FMS-like tyrosine kinase 3 (FLT3)-mutant acute myeloid leukemia (AML), in which Cao et al. found that nonclassical NF-κB signaling induced the expression of CXCL1, CXCL5, and CXCL8 to promote resistance to gilteritinib [61]. Here, CXCL1 is linked to acute myeloid leukemia.