GJA1 and atherosclerosis: Their results revealed that disturbed flow and OSS can phosphorylate and activate mammalian sterile 20‐like kinase 1 (MST1), which in turn phosphorylates and activates its downstream protein connexin 43 (CX43), leading to conformational changes in CX43 and increased immune cell infiltration, ultimately accelerating the development and progression of atherosclerosis.[25] Similar to the present study, their research focused on the mechanisms by which OSS leads to vascular endothelial dysfunction and atherosclerosis.