The conjunction of these findings with the data already presented in the bungarotoxin-induced MG rat model, where no evidence of significant damage of muscle integrity have been reported [7, 36] suggests that a decreased accumulation of adenosine leading to insufficient tonic activity of A2AR on motor endplates of myasthenic animals may be linked to muscle paralysis caused by the loss of nAChR, instead of the immune mediated disruption of endplate morphology. The gene discussed is ADORA2A; the disease is myasthenia gravis.