Since S1P1FloxFoxp3Cre mice have autoimmunity, it is possible that the increased number of effector Treg cells that we observed in the S1P1FloxFoxp3Cre mice could be the result of systemic inflammation and does not necessary imply that S1P1 regulates the transition from cTreg to eTreg. The gene discussed is S1PR1; the disease is Autoimmunity.