FASN and chronic obstructive pulmonary disease: These conflicting observations could be attributed to a number of factors, including a loss in total AEC2 cell numbers in the lung after smoke (reflected by lower SFTPC levels), with those remaining viable AEC2 cells demonstrating increased adaptive FASN expression, or a loss of FASN in other cell types including fibroblasts, endothelial cells, and infiltrating macrophages, all of which play a role in COPD pathogenesis (4, 53).