This dysfunction in neutrophil activity generates greater inflammation and a non-resolving host response (continuous inflammation) to the infection (Cox et al., 1995; Alhede et al., 2014), contradicting the normal course of healing which requires dampening of pro-inflammatory cytokines, such as IL-1β, IL-6, and IL-8, and increased levels of anti-inflammatory cytokines, like IL-10 (Ding et al., 2015). The gene discussed is IL1B; the disease is infection.