A recent survey of 25 CLN2 cases in South America showed that patients with a more severe phenotype (the classical form) had null TPP1 activity, while the group of patients with residual TPP1 activity showed later onset and longer life‐span, with slower progression, less epilepsy syndrome and a higher frequency of ataxia particularly at a late stage of the disease.2 The gene discussed is TPP1; the disease is epilepsy syndrome.