It is thus assumed that the tumor-promoting effect of silica dust is mediated by TGF-β, mitigating the function of FasL towards a decreased release of cytokines or chemokines that are crucial for antitumor immunity, and causing a shift in FasL-associated activities from an inflammatory to a suppressive function, so that the removal of silica-induced transformed cells is largely impeded (150). The gene discussed is FASLG; the disease is neoplasm.