The attributable proportion due to the interaction between the TNFRSF1B rs1061622 genotypes and smoking was estimated to be 0.49 (95% CI: 0.07–0.92), suggesting that 49% of the excess risk for SLE in smokers with at least one G allele was due to an additive interaction [38]. The gene discussed is TNFRSF1B; the disease is systemic lupus erythematosus.