However, considering the fact that EBV is known to cause pleiotropic interactions with host inflammatory responses, and in the present case, played a crucial role in the development of SLE clinically, we hypothesize that EBV infection might have altered the immune response and contributed to the pathogenesis of the lung lesions through aberrant T cell responses, dysregulated IFN and other cytokines responses, and dysfunctional CD8 responses [2,3,6,7]. Here, IFNA1 is linked to systemic lupus erythematosus.