Although natural ligands belonging to T2 inflammation, such as IFNγ, IL-5, IL-3 and IL-13 activates JAK/STAT signaling in innate immunity and can be inhibited using pan-JAK inhibitors14, other common bacterial mediators present in COPD and severe asthma, such as LPS, can trigger JAK2 and STAT3 phosphorylation in macrophages35,36. The gene discussed is SOAT1; the disease is asthma.