Indeed, drug experiments using, for example, NSAIDs, revealed that GDF‐15 and COX‐2 expression are inversely regulated.41 Furthermore, our data support the notion that increased numbers of COX‐2+ cells in atherosclerotic lesions of GDF‐15−/−/apoE−/− may play an antiatherosclerotic role, as already supposed by others.42 Conversely, it has been demonstrated that COX‐2 deficiency results in a marked elevation of proinflammatory cytokines like IL‐6.42 Our data suggest that IL‐6 plays a major role in the progression of atherosclerosis and is a putative target of GDF‐15. Here, PTGS2 is linked to atherosclerosis.