Alzheimer's, Parkinson's, Huntington's diseases, amyotrophic lateral sclerosis (ALS), and gliomas have been linked to self‐templating forms of specific amyloid deposits: Amyloid β and tau in Alzheimer's, α‐synuclein in Parkinson's, huntingtin in Huntington's diseases, TDP‐43 in ALS, and GLIPR2 in gliomas. Here, GLIPR2 is linked to juvenile Huntington disease.