In addition, in a pancreatic cancer model, where IL17A signaling enhances neutrophil recruitment and NET formation, inhibition of PAD4, an enzyme needed for NETosis that supports chromatin decondensation by citrullination of histone 3 [15], or IL17A blockade reverts CD8+ T-cell exclusion from the tumor mass and sensitizes to anti-PD-1 plus anti-CTLA-4 treatment [16]. The gene discussed is IL17A; the disease is neoplasm.