For example, PKC θ-deficient mice (PKC θ−/−) have reduced incidence and severity of Th2 and Th17-mediated inflammatory disorders, including asthma, inflammatory bowel disease, multiple sclerosis, arthritis, and allograft rejection in comparison to their wild-type littermates (PKC θ+/+; Marsland and Kopf, 2008; Zanin-Zhorov et al., 2011; Altman and Kong, 2012). The gene discussed is PRRT2; the disease is arthritic joint disease.