Cancer progression is associated with the release of inflammatory cytokines, including IL-6 and IL-23, which might promote further growth of the tumor cells in a microenvironment dominated by STAT3 signaling. However, the same cytokines in combination with TGF-β might be involved in polarizing tumor-infiltrating lymphocytes into type 17 cells. The IL-17 produced by infiltrating T cells may have multiple proinflammatory effects. Importantly, Th17 CD4⁺ T cells can be unstable and evolve into IFN-γ–producing Th1-like cells capable of tumor destruction.⁷  A similar pathway is postulated for CD8⁺ IL-17–producing cells (Tc17) evolving into cytotoxic effectors (Tc1).¹²