Notably, a few studies have shown that FGF14 expansions in the incompletely penetrant range (250–299 GAA repeats) may co-occur with other pathogenic variants associated with hereditary ataxias.14,15 In those cases, the clinical phenotype usually reflected the co-occurring variant with earlier onset and a more severe or complex presentation that deviated from the classic SCA27B phenotype. This evidence concerns the gene FGF14 and Rare hereditary ataxia.