Furthermore, during left ventricular remodelling after MI, S1PR1 and S1PR3 promote the recruitment of γδT cells to the infarcted heart to produce IL‐17A and then stimulate macrophages to produce pro‐inflammatory cytokines such as TNF‐α, IL‐6, IL‐1β, CCL2, MMP9 and CXCL1, thereby aggravating myocardial cell death and fibroblast proliferation, indicated by the increased expression of fibrosis genes such as TGF‐β, collagen 1, collagen 3 and periostein (Figure 2B).43 This evidence concerns the gene S1PR1 and myocardial infarction.