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. Here, SOAT1 is linked to chronic obstructive pulmonary disease.