Numerous studies have shown that IL‐38 can not only down‐regulate HIF‐1α70 but also inhibit the expression of β‐glucan‐induced trained immune‐related genes (Tnfa, Nrlp3, Hk2, and Pfkp) and inflammation by blocking the mTOR signaling pathway, thereby limiting the inflammatory response in atherosclerosis.132. Here, IL1F10 is linked to atherosclerosis.