An experiment in mice reported that loss of T-bet promoted IL-17 production and caused autoimmune myocarditis.[9] In humans, the T-bet levels have been shown to increase with age.[10] Mormile speculates that, in addition to low T-bet expression in young people, T-bet polymorphisms may generate autoreactive CD8 cells that increase the likelihood of myocarditis.[11] Estrogen may upregulate T-bet expression, making myocarditis less likely.[12]. The gene discussed is CD8A; the disease is autoimmune myocarditis.