Mice lacking ORAI1 manifest reduced enamel mineralization (Robinson et al., 2012) and thinner skin with elongated keratinocytes and smaller vibrissae follicles (Gwack et al., 2008), and the ectodermal-specific knockout of Orai1 or Stim1/Stim2 impairs SOCE and results in anhidrosis and a reduced sweat gland lumen (Concepcion et al., 2016). The gene discussed is STIM1; the disease is anhidrosis.