The main etiology of infections as a trigger factor for SLE is pathogen-induced abnormal immune responses, such as upregulation of the type I interferon (IFN) system and superantigen production, leading to activation of T lymphocytes (Barbhaiya and Costenbader, 2016; Pan et al., 2019). The gene discussed is IFNA1; the disease is systemic lupus erythematosus.