They identified a possible gene×environment interaction, where smokers with the slow acetylator genotype of NAT2 were found to have a higher risk of SLE (Odds Ratio = 6.44, 95% CI = 3.07–13.52) when compared to non-smokers with the rapid acetylator genotype of NAT2. Our study was the first to find passive smoke exposure as a child (childhood exposure to secondhand smoke) to be a significant risk factor for SLE. The gene discussed is NAT2; the disease is systemic lupus erythematosus.