Conciliating these new findings with the observation that vertebral trabecular bone of α2C-AR−/− mice shows resistance to thyrotoxicosis after 4 and 12 weeks of T3 treatment (44), we could suppose that α2C-AR signaling is the main α2-AR subtype to mediate TH actions on trabecular bone of the vertebra until 4 weeks of thyrotoxicosis, but that, in longer situations of thyrotoxicosis (12 weeks), α2A-AR signaling could also contribute to the detrimental effects of TH excess. This evidence concerns the gene ADORA2A and thyrotoxicosis.