In the context of autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), the crosstalk between IFN-I and TNFα is hypothesized to be of crucial importance, as literature suggests an inhibitory effect of TNFα on IFN-Is, and vice versa (30, 31). The gene discussed is TNF; the disease is systemic lupus erythematosus.