STAT3 promotes the transcription of lnc-M2 and upregulates the epigenetic histone modification marker at the promoter of lnc-M2, which suggested that STAT3 activates lnc-M2 and promotes the differentiation of M2 macrophages through the protein kinase A (PKA)/cAMP response element binding protein (CREB) pathway, ultimately mediating the core role of macrophages in the pathogenesis of asthma and allergy, tumorigenesis, and atherosclerosis [22] (Fig. 2). Here, STAT3 is linked to atherosclerosis.