Nevertheless, the cross-talk between our previous data on human primary cells and the actual data on an animal model is the level of IL-1-like cytokines (i.e., IL-1α, IL-1β, and IL-33), which are related to the inflammasome complex activation, most likely associating lung immunosuppression to pro-fibrotic processes, as observed in other respiratory diseases (24, 25). The gene discussed is IL33; the disease is respiratory system disorder.