ADORA2A and myasthenia gravis: Failure of this mechanism has been associated with neuromuscular transmission deficits in myasthenic patients, leading us to hypothesise that targeting the endogenous ADO formation by ecto-5′-nucleotidase/CD73 and A2AR activation might restore neuromuscular competence while also suppressing activation of the immune system in myasthenia gravis patients [28, 69, 114].