Patients hospitalized for Covid‐19 severe infection are more prone to excessive coagulation activation leading to thrombotic events. Tang et al1 discussed the importance of high D‐dimer and fibrin degradation product level to determine the patient prognostic and the risk of thrombosis. However, they did not look at lupus anticoagulant (LAC). Zhang et al described three cases of thrombosis associated with antiphospholipid antibodies represented by anticardiolipin (aCL) and anti–β2‐glycoprotein I (aβ2GPI).2 No lupus anticoagulant was detected in any of the patients. During the recent Covid‐19 outbreak in Mulhouse, France, we have studied 56 patients diagnosed for Covid‐19 using polymerase chain reaction (n = 50) or chest computed tomography scan (n = 6), for the presence of LAC with dilute Russell’s viper venom time and sensitive activated partial thromboplastin time tests. Twenty‐five cases (45%) were LAC positive, whereas aCL or aβ2GPI were detected in only five of 50 tested patients (10%, three associated to LAC) using immunoglobulin G and immunoglobulin M detection. Acute infections are known to be sometimes associated with transient LAC, and anticoagulant therapy is usually not needed.3 Detection of LAC with or without aCL or aβ2GPI, in these critically patients, which are characterized by having many thrombosis risk factors, highlight the importance of an early anticoagulant therapy.