In previous studies using mouse models with transgenic overexpression or systemic infusion, Vpr was shown to block the expression of peroxisome proliferator–activated receptor γ but to stimulate glucocorticoid receptor-mediated signaling, resulting in dysfunction of fat metabolism that manifested as accelerated whole-body lipolysis, hyperglycemia, hypertriglyceridemia, and hepatosteatosis (69). Here, NR3C1 is linked to hypertriglyceridemia.