After lung cancer formation, TAMs in the tumor microenvironment induce M2 polarization through a series of complex molecular mechanisms, including the COX-2/PGE2/EP4 signaling axis, the AMPKα1/STING positive feedback regulatory pathways, the regulatory role of Zeb1 transcription factors, the involvement of CtBP1, the mediation by CCL2, and the secretion of circFARSA or the release of exosomes carrying PD-L1 (39–45). This evidence concerns the gene PRKAA1 and lung carcinoma.