On 4 February 2020, a 67-year-old man, with a medical history of chronic obstructive pulmonary disease, hypertension, and diabetes presented to the hospital with a 1-week history of cough, fatigue, and sputum with fever. Temperature (T) was 37.5°C; CURB-65 score was 3. White blood cell count 3.33 × 1012/L, lymphocyte absolute value 0.55 × 109/L, procalcitonin 16.66 μg/L, C-reactive protein (CRP) 16 mg/L, interleukin (IL-6) 357.3 pg/mL (0-7 pg/mL), and IL-6 level were measured by using the ELISA method. Computed tomography (CT) scan showed progressive infiltrate and diffuse gridding shadow in both lungs. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) test was positive. The patient received oseltamivir and lopinavir plus ritonavir as antiviral therapy and methylprednisolone to alleviate lung inflammation. On day 3, his vital signs were unstable: respiratory rate (RR) 30 breaths/min, heart rate (HR) 113 beats/min, blood pressure (BP) 120/70 mmHg, SpO2 88% (oxygen 3 L/min), and T 39.5, and oxygenation index was down to 108; he was transferred to intensive care unit immediately and received high-flow nasal cannula oxygen therapy (55% concentration, flow rate 40 L/min). On day 4, RR increased to 35 breaths/min and oxygen saturation decreased to 70%, and then he was changed to invasive mechanical ventilation (MV). The noradrenaline was started with a dose of 0.30 μg kg−1 min−1. On day 15, the tracheostomy was performed due to prolonged duration of MV support. Plasma exchange was performed using the Diapact CRRT system, and a filter membrane-based apparatus (BBraun, Melsungen, Germany) through the extracorporeal system and therapeutic plasma exchange (TPE) set was used. Fresh frozen plasma was used as the replacement fluid, and the total amount was 3000 mL. We did not have a protocol or consensus in treating coronavirus disease (COVID-19) patients with TPE, and we also did not get “cut-off” values or indications; the TPE treatment was started depending on the initiative and experience of the critical care staff. In this case, TPE was administered for 2 hours a day for 3 consecutive days. In order to make sure the antibiotics, antiviral, antifungal drugs, and other drugs were not cleared by TPE, they were given after the completion of TPE. After three sessions of TPE, the serum IL-6 level was decreased from 3815 pg/mL to 286.9 pg/mL, and CRP decreased from 50.2 mg/L to 19.6 mg/L. The chest CT revealed improvement of both lungs (Figure 1). The circulatory efficiency significantly improved, and noradrenaline was discontinued. In the pathophysiological progress of COVID-19 patients and following secondary infection, it was shown that pro-inflammatory cytokines were dramatically increased in the patients with COVID-19 and the plasma cytokine concentrations were much higher in critical patients.1 The inflammatory cytokine storm may occur when cytokines reach a certain threshold in the patients.2 Inflammatory cytokine storm and immunopathology through the dysregulation of chemokines and cytokines resulted in the apoptosis of epithelial and endothelial cells, caused vascular leakage and infiltration of macrophages and neutrophils, which together induced severe lung injuries.3 One study showed that some COVID-19 patients deteriorated in the later stage and soon went into the state of multiple organ dysfunction, which correlated with the sudden initiation of an inflammatory cytokine storm in critical patients.4 Similarly, our study informed that in this case report, the COVID-19 patient had a sustainable high concentration of IL-6. It has been proposed that IL-6 > 100 pg/mL could represent the appearance of inflammatory cytokine storm. The potential limitations were large amounts of FFP are needed for every treatment, some drugs are depleted incalculably, and SARS-CoV-2 antibodies were also removed from the patient's serum.5 However, TPE would be still prescribed as an important treatment in alleviating inflammatory cytokine storm when needed in COVID-19 patients.