Taken together, these data suggest that loss of STAT3 in the tumour cells results in increased CXCL1/IL-8 expression triggering infiltration of myeloid cells as well as augmented vascularization, and identifies CXCL1/IL-8 as an essential mediator for the accelerated development and progression of Stat3-deficient tumours. Here, CXCL8 is linked to neoplasm.