For instance, production of alternative pro-angiogenic factors, such as fibroblast growth factors (FGFs) and placenta growth factor (PlGF), or downregulation of angiostatic chemokines, such as Cxcl9, or induction of pro-inflammatory cytokines, that is, IL-1, IL-6, TNF-α, by tumor cells have been implicated in the mechanisms of TKI resistance30–32. This evidence concerns the gene CXCL9 and neoplasm.