We initially observed that our in-house bred specific-pathogen-free herpesvirus entry mediator (HVEM)-deficient mice (HVEM−/−) had higher fasting blood glucose, worse glucose intolerance during glucose tolerance testing (GTT), and increased gluconeogenesis during pyruvate tolerance testing (PTT) compared to wild-type (WT) mice obtained from Vital River Laboratory Animal Technology (VRL) (see Fig. S1 in the supplemental material). The gene discussed is TNFRSF14; the disease is Glucose intolerance.