Libman-Sacks endocarditis (LSE) is a rare disease found incidentally in ‎postmortem autopsies, characterized by microscopic to large ‎verrucous vegetation on the cardiac valves, the most affected site is ‎the mitral valve followed by the aortic valve. Females of reproductive age ‎were observed as the most affected individuals as found in studies. ‎Most individuals with LSE are asymptomatic and ‎generally discovered lately when they presented with ‎thromboembolic disorders such as stroke, cognitive disabilities, and death. ‎Malignancy and autoimmune diseases involving systemic lupus ‎erythematosus (SLE) and antiphospholipid syndrome (APS) are ‎considered the primary etiology of LSE. As recognized, the majority of LSE cases are ‎asymptomatic, it tends to be challenging to spot the condition ‎at the early pathway of the disease. In this paper, we describe a ‎young female who is known to have SLE on medications, she presented ‎to the emergency department (ED) due to chest pain and exertional ‎dyspnea for a few days, laboratory investigations showed ‎anemia, raised inflammatory marker, and anti-DsDNA. Imaging ‎studies showed bilateral pleural effusion on the chest X-ray ‎and a large vegetation on the posterior mitral valve with moderate regurgitation and normal wall ‎motion in transesophageal echocardiography. The patient was managed by pulse steroid therapy, anticoagulation ‎therapy, and a low dose of diuretic, the patient improved dramatically and ‎discharged home with close follow-up in the clinic. The primary ‎treatment of LSE is anticoagulant therapy, however, surgical ‎intervention should be considered in case of large vegetation ‎recurrent thromboembolism despite anticoagulant therapy. As ‎the prognosis in LSE is considered very poor and there is no definitive laboratory investigation ‎exists to confirm the diagnosis, we highlight the importance of ‎considering LSE as a serious and crucial differential diagnosis ‎when dealing with SLE patients who presented with dyspnea and pleural effusion secondary to valvular dysfunction, mainly the mitral valve.