Several lines of evidence indicate that different molecular and cellular mechanisms participate in the reciprocal action between ISCs/CSCs and inflammatory mediators, involving the release of inflammatory cytokines (interferons (IFNs), tumor necrosis factor (TNF), IL-6, IL-17) and the activation of inflammatory cells, such as myeloid-derived suppressor cells and tumor-associated macrophages [97]. Here, IL17A is linked to neoplasm.