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Introduction: The ATTACH trial in 2003 demonstrated that Anti-tumor necrosis factor alpha therapy was associated with the evolution and progression of heart failure in patients with moderate to severe chronic heart failure. The United States FDA also reports that in rare cases, it is implicated in new onset heart failure in those under the age of 50. We present a case of new onset biventricular failure with cardiogenic shock in the setting of anti-TNF therapy, resulting in orthotopic heart transplantation. Case: A 22-year-old male with history of Crohn’s disease, on infliximab, presented to the ED with dyspnea. He was recently hospitalized for right middle cerebral artery CVA, during which he was diagnosed with new onset nonischemic cardiomyopathy with an LVEF 26% on cardiac MRI. Extensive workup was unrevealing for etiology of cardiomyopathy. He had a negative 3 generation family history to suggest familial or inherited cardiomyopathy. In the ED, he was hypotensive at 62/41 mmHg, tachycardic to 104 bpm. Laboratory data demonstrated a lactate 11.5 mmol/L, creatinine 1.96 mg/dL, AST 454, ALT 670, total bilirubin 1.3, and NT Pro-BNP 6607 pg/mL. A pulmonary artery catheter was placed, which revealed RAP 28 mmHg, PCWP 26 mmHg, PAPI 0.7, Fick CI 1.1 L/min/m 2 and CPO 0.41 W. A shock alert was called, and the patient was emergently cannulated for V-A ECMO with an IABP for LV venting. He was transferred to a transplant center, where he underwent OHT. Discussion: Anti-TNF therapy has been implicated in the worsening of chronic heart failure; however, the development of new-onset heart failure is rare, and the literature is limited. Kwon et al reported a case series from the FDA MedWatch list, which included 47 patients who experienced new or worsening heart failure after starting Infliximab or Etanercept for ulcerative colitis, rheumatoid arthritis, and psoriatic arthritis. Of these 47 patients, 38 (81%) developed new onset heart failure. The pathogenesis of heart failure in patients on TNF alpha therapy is thought to be related to a dose-dependent activation of the Death-promoting pathway mediated by TNF Receptor 1 and a relative decrease in activation of the Survivor Activating Factor Enhancement pathway mediated by TNF Receptor 2. We add this case to the growing body of literature regarding the risks of TNF-alpha inhibitors in patients with established heart failure and propose using TNF-alpha inhibitors as the etiology of this patient’s new onset cardiomyopathy.