Furthermore, Seifert et al. [64] reported that the in vivo deletion of RIPK3 or RIPK1 attenuated tumor progression and immunosuppression in mice and explained these results by suggesting that necroptosis promoted pancreatic oncogenesis because CXCL1 (chemokine (C-X-C motif) ligand 1), which is a chemokine attractant, and Mincle signaling induced by necroptosis promotes the induction of adaptive immunosuppression by myeloid cells. The gene discussed is RIPK3; the disease is neoplasm.