The administration of gemcitabine and 5-FU on MSC-2 cells, an established myeloid-derived suppressor (MDSC) cell line, led to the activation of NLRP3 via lysosome permeabilization and cathepsin B release enhancing an IL-1β-dependent T helper 17 (Th17) response, which limited the anti-cancer efficacy due to a proangiogenic effect [54] (Figure 1b, Table 1). The gene discussed is NLRP3; the disease is cancer.