Emerging mechanistic studies in non-TB models provide plausible hypotheses: CD274 (PD-L1) promotes NET release via PI3K/Akt/mTOR signaling in endotoxin-induced lung injury (60), IRF1 drives ROS-dependent NETosis in LPS-challenged neutrophils (61), HPSE facilitates NET extrusion through heparan sulfate cleavage in cancer-associated inflammation (54, 59). Here, AKT1 is linked to tuberculosis.