This hypothesis is further complemented by the M2 polarization profile (APOE, TXN, TGM2, STING1, NAMPT) enriched in this group, a dominant macrophage profile in high Th2-type asthma in humans and one known to activate the Th2 response with downstream eosinophilic infiltration and airway remodeling [54]. The gene discussed is APOE; the disease is asthma.