IMCAs are divided into two groups: (1) those in which the trigger of autoimmunity leading to cerebellar damage are known, such as infection (e.g., post-infectious cerebellar syndrome, PiCS, post-infectious cerebellitis), neoplasm (e.g., paraneoplastic cerebellar degeneration, PCD), and gluten sensitivity (gluten ataxia, GA); and (2) those with no clear triggers but with serological markers strongly suggestive of IMCAs (e.g., anti-GAD ataxia). This evidence concerns the gene GAD1 and paraneoplastic neurologic syndrome.