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A 57 year-old woman was admitted with acute dysarthria and dysphagia on a background of Sjogren’s syndrome with triple-positive antiphospholipid syndrome (APLS) and metastatic endometrial cancer. She had incurred several thromboembolic events over three years including splenic infarct, pulmonary embolism, and in the final eleven months sustained three ischaemic MCA infarcts (each with successful thrombectomy). These events occurred despite therapeutic anticoagulation and hydroxychloroquine therapy. Hitherto the aetiology for her morbidity was attributed solely to APLS, as an unrevealing and singular index echocardiogram had been completed at the time of her first cerebrovascular accident.This admission the patient underwent M1 endovascular thrombectomy, with an improvement in NIHSS from 11 to 2. Histopathology demonstrated platelet/fibrin-rich thrombus with low erythrocyte count. FBC revealed pancytopenia whilst coagulation times were normal with an elevated D-Dimer and non-consumed fibrinogen. Repeat assays for antiphospholipid antibodies were remarkably negative, however transthoracic echocardiography demonstrated a small echogenic mass on the anterior mitral leaflet with concomitant, new mild regurgitation. Blood cultures remained negative throughout admission.Haematology input was sought before a diagnosis of marantic (non-bacterial thrombotic) endocarditis was made. Therapeutic enoxaparin was re-introduced 24 hours post-thrombectomy, and methylprednisolone pulse was initiated. Hydroxychloroquine was re-commenced, and the patient received a four-week course of rituximab. Three months later she remains on therapeutic enoxaparin without further thromboembolic events.This case reminds us to consider marantic endocarditis as a cause of recurrent multi-territory infarcts with echocardiographic (but not microbiological) findings, and to avoid diagnostic overshadowing amidst systemic inflammation and malignancy.