In this regard, smoking-associated asthma is considered a T2-low neutrophilic phenotype speculating that persistent exposure to cigarette smoke may induce a predominance of activated macrophages producing proinflammatory molecules, reactive oxygen species, matrix metalloproteinases, and specific chemokines such as IL-8, contributing to the prolonged survival of neutrophils in the lung tissue [67]. The gene discussed is CXCL8; the disease is asthma.