Hyperinflammation can result from overproduction of IFN-γ with downstream pro-inflammatory cytokines, such as tumor necrosis factor (TNF)a, interleukin (IL)-1, IL-18, and others; studies have demonstrated serious hyperinflammatory and immune-mediated diseases, which include autoinflammatory diseases, cytokine storm, and other.35 Given the potential for deleterious effects of excess inflammation and clinically beneficial correlation of higher IFN-γ and GzB levels with clinical influenza infection and post-vaccination, these data warrant further research.15,35–38. This evidence concerns the gene IL18 and influenza.