AIM2 and chronic obstructive pulmonary disease: The smoking effects on T cell responses persist years after individuals quit smoking, highlighting a mechanism for the persistent effects in the adaptive response associated with DNA methylation at signal trans-activators and metabolism regulators [53]; (g) Inflammation and ROS production: inflammasomes (leucine-rich repeat (LRR)-containing proteins (NLR) family members such as NLRP3, NLRP6, NLRP12, and interferon-inducible protein (AIM2)) may contribute to the development of various diseases associated with cigarette smoke exposure, including COPD.