We have shown that IRAK4 inhibition significantly reduced the recruitment of neutrophils, specifically the N5 subset, and MoAM as well as key MoAM- and neutrophil-associated inflammatory mediators such as CCL2/CCL7 and IL-1β/TNF-α that are required to establish and maintain (smoke-induced) pulmonary inflammation and tissue remodeling/emphysema (12, 22, 72). Here, IL1B is linked to pulmonary emphysema.