Horie et al. [5] once reported that mice with the BALB/c genetic background developed hyperthyroidism regardless of whether the IL-17 gene was knocked out; however, some wild-type but not IL-17 knockout NOD.H-2h4 mice experienced hyperthyroidism, indicating that IL-17 functions can depend on the genetic background of the species. The gene discussed is IL17A; the disease is hyperthyroidism.