In a very recent study, we confirmed the upregulation of Alox5 in pro-inflammatory MΦs, revealing a new and unique role for Alox5 in producing leukotriene B4 (LTB4) as a driver of ferroptotic cell death in ATII cells in both COPD patients and animal models.4 This evidence concerns the gene ALOX5 and chronic obstructive pulmonary disease.