CSF3 and neoplasm: In syngeneic tumor pre-clinical models, Chung et al. [13] well described how IL-17A is implicated in a network that favors tumor escape following anti-VEGF treatment, notably via an IL17/G-CSF (granulocyte colony-stimulating factor)/Bv8 (prokineticin-2) alternative pathway initiated by Th17 infiltration.