Although the role and potential mechanism of IL‐38 after IS have not yet been reported, considering that atherosclerosis is the main cause of IS development, combined with IL‐38 is negatively correlated with pathological damage after IS, we speculate that IL‐38 is likely to affect pathological injury after IS by regulating immune cells, inflammatory response, and apoptosis, however, its specific mechanism remains to be elucidated (Figure 3). The gene discussed is IL1F10; the disease is atherosclerosis.