Chung et al.33 also showed that IL-17 signaling cascade mobilizes the granulocyte colony-stimulating factor (CSF)-dependent recruitment of CD11b+Gr1+ immature myeloid cells, which acts as major driving force for anti-VEGF tumor refractoriness.34 Mostly, the role of EphA2/EphrinA1 signaling has been attributed with compensatory angiogenesis and concerned tumor resistance. This evidence concerns the gene CSF3 and neoplasm.