This anti‐myocarditis activity of S1P was further confirmed by Kitabayashi et al who observed that the activation of S1PR1 and S1PR3 by the non‐selective agonist fingolimod prevented the development of experimental autoimmune myocarditis in rats, and fingolimod was more effective in this aspect than the immunosuppressive drug tacrolimus,46 proving the therapeutic potential of S1P in human myocarditis. The gene discussed is S1PR1; the disease is myocarditis.