Denny et al. reported that LDGs in SLE patients had an augmented capacity to damage endothelial cells and synthesize proinflammatory cytokines (e.g. IFN-α, TNF-α, and IFN-γ) compared with autologous NDNs from lupus patients and HCs [14]. The gene discussed is IFNG; the disease is systemic lupus erythematosus.