Zhang et al found that after MI, cardiac S1P was increased, and the SphK1/S1P/S1PR1 signal in myocardium was amplified, accompanied by the presence of pro‐inflammatory transcription factors NF‐κB and STAT3 and pro‐inflammatory cytokines TNF‐α and IL‐6 as well as then the up‐regulation of remodelling genes ANP, BNP and β‐MHC, indicating that the SphK1/S1P/S1PR1 signalling activates myocardial inflammation and exacerbates cardiac remodelling and dysfunction post‐MI.42 The gene discussed is STAT3; the disease is myocardial infarction.