Based on the concept that COPD is characterized by lung fibrosis associated with remodeling of small airways (Barnes, 2014) and that IL-1-like cytokines are involved in this process (Borthwick, 2016), and because we already found that the activation of the AIM2 inflammasome is involved in a pro-fibrotic process (Terlizzi et al., 2018b), we evaluated whether AIM2-dependent IL-1α release in COPD-derived PBMCs were impaired after treatment with two different anti-fibrotic drugs (Halwani et al., 2011). Here, IL1A is linked to chronic obstructive pulmonary disease.