These observations suggest that chronic presence of proinflammatory cytokines such as TNFα + IL-1β at the tumor microenvironment (TME) drives TNBC cells into a prometastatic phenotype, in a manner that has not been reported previously; such a persistent proinflammatory stimulation can modify through metabolic upregulation the expression of inflammatory mediators that indirectly, through the recruitment of deleterious monocytes and neutrophils, may increase the prometastatic phenotype of TNBC cells. This evidence concerns the gene IL1B and neoplasm.