Treg-specific genetic ablation of Mcu (Mcufl/flFoxp3Cre mice) did not lead to an overt spontaneous immune reaction in mice not subjected to an additional disease model nor did challenging the Mcufl/flCD4Cre mice in experimental autoimmune encephalomyelitis (EAE) or lymphocytic choriomeningitis virus (LCMV) infection models [8], indicating that MCU is dispensable for function of Tregs, but permanent MCU ablation may be compensated by other Ca2+ influx mechanisms in vivo. The gene discussed is MCU; the disease is experimental autoimmune encephalomyelitis.