A patient, a 15-month-old male castrated Goldendoodle, presented to the Cornell University Hospital for Animals (CUHA) Neurology Service for a chief complaint of a 10-day history of regurgitation, vomiting, and coughing and a 2-day history of progressive weakness, especially in the pelvic limbs. Mechanical obstruction had been ruled out by the primary care veterinarian prior to presentation to the CUHA and the dog had been treated empirically for gastrointestinal upset and esophagitis with supportive care. His signs seemed to improve for a few days before relapsing. Neurologic examination revealed sternal recumbency, an ability to rise for less than 2 seconds before exhaustion, and fatigable palpebral reflexes. General physical examination revealed tachypnea and harsh lung sounds ventrally, raising concerns for aspiration pneumonia due to his recent history of regurgitation. Point-of-care bloodwork revealed an elevated alveolar to arterial (A-a) gradient and a respiratory alkalosis. Thoracic radiographs revealed a diffusely dilated esophagus and increased opacity within the left cranial lung lobe over the cardiac silhouette. Due to the multifocal nature of the patient’s weakness, the presence of megaesophagus, and an otherwise normal neurologic assessment, a presumptive diagnosis of acquired myasthenia gravis was made. An acetylcholine receptor antibody (AChRAb) titer test was sent out for confirmation. Treatment options for acquired myasthenia gravis primarily involve lifelong supportive care, acetylcholinesterase inhibitors (e.g. pyridostigmine) to prolong the action of acetylcholine, and immunomodulatory drugs (e.g. mycophenolate and azathioprine) to control the suspected autoimmune component of the disease process. This seminar will review the presentation, pathophysiology, diagnosis, treatment, and prognosis of small animal veterinary patients with acquired myasthenia gravis.