In contrast, the T1D clinical trial directly intervened to reduce and maintain stably reduced co-stimulatory molecules CD40, CD80, and CD86 without the use of an NF-κB inhibitor, but other than demonstrating low IL-12 concentrations during stimulation in vitro, it did not further characterize the generated tDC beyond purity and sterility. The gene discussed is CD80; the disease is type 1 diabetes mellitus.