Animal studies further elucidated this; for example, mouse models showed cerebellar inflammation and T-cell infiltration in 84% of mice treated with anti-CTLA-4 antibodies, expressing a neo-self-antigen in Purkinje and tumor cells, compared to no inflammation in controls, implicating T-cell dysregulation in neurologic toxicities [83]. This evidence concerns the gene CTLA4 and neoplasm.