Similar studies in SCA2 revealed stability in repeat expansion due to presence of CAA interruptions in PMNAs and deviation from typical ataxic phenotype to other clinical manifestations like parkinsonism, etc.[38, 48, 60] Studies have also revealed the risk for amyotrophic lateral sclerosis (ALS) associated with large normal CAG repeats in ATXN2. The gene discussed is ATXN2; the disease is Parkinsonism.