The same study also detected that more proinflammatory molecules, such as interferon β and interleukin-1β were produced in the selenium-deficient group because multiple genes involved their upstream pathways, including UPS18, DDX58, cGAS, and TLR3 were upregulated, which further supported the conclusion that selenium deficiency could resulted in mitochondrial DNA damage and disorder energy production of cardiac cells (169). The gene discussed is TLR3; the disease is selenium deficiency.