Although indirect effects of EPO on whole body metabolism cannot be entirely excluded, the EpoRaP2KO mouse model with fat specific knockout of EpoR suggested that the loss of EPO/EpoR signaling in adipose tissue is sufficient to develop the metabolic syndrome phenotype including obesity, glucose intolerance and insulin resistance and supports the idea that EPO activity in fat may contribute to energy homeostasis. The gene discussed is EPOR; the disease is Glucose intolerance.