We do not know, yet.13,14 However, in vitro studies showed that HCQ blocks viral replication by inhibiting the entry of SARS-CoV-2 by interacting with glycosylation of angiotensin converting enzyme-2 (ACE-2) receptor and its binding with the spike protein.18 This remains to be documented and there are some trials that are trying to support it.19–21 Furthermore, high HCQ blood levels are associated with reduced thrombotic events in SLE patients,22 which is also a clinical manifestation of SARS-CoV-2 patients. The gene discussed is ACE2; the disease is systemic lupus erythematosus.