While elevated IL-6 could contribute to the development of protective Th17 response after recognition of exposed fungal epitopes, hyperinflammation of the IL-17 axis and excessive neutrophilic influx are also risk factors, and recent work suggests that myeloid-derived suppressor cell-mediated immunomodulation is protective during this phase around 4–7 days post-infection [54–58], [59]. The gene discussed is IL17A; the disease is infection.