The anti-tumor activities of ACKR1 were mediated not only by reducing microvessel density, but also by inhibiting atypical cancer-related activities, such as MMP9 production and tumor cell proliferation, as well as increasing tumor cell senescence (192, 194–196); from the mechanistic perspective, it was demonstrated that ACKR1 caused anti-tumor effects by interfering with CXCR2-induced STAT3 activation in pancreatic adenocarcinoma cells (192). This evidence concerns the gene STAT3 and neoplasm.