To extend these observations to physiologically relevant settings in vivo, Wang and colleagues next employed adoptive transfer of RyR2-deficient Tconvs (versus wild-type Tconvs or wild-type Tregs) into multiple immune-mediated disease models, including infection or inflammatory models (herpes simplex virus-1 infection, ovalbumin-induced [OVA-induced] airway inflammation, and dextran sulfate sodium–induced colitis), a cancer model (MC38 adenocarcinoma), and an autoimmune model (scurfy mice). This evidence concerns the gene RYR2 and cancer.