Lack of EpoR in nonhematopoietic tissues did in no way impair the efficacy of hypoxia and rhEPO to ameliorate hyperglycemia, glucose intolerance, and insulin resistance, clearly implicating that direct EPO action on nonhematopoietic tissues was not required for glucose lowering (Fig. 3, D, E, I, and J). The gene discussed is EPO; the disease is Insulin resistance.