We have recently found that deficits in the brain-derived neurotrophic factor (BDNF)–tropomyosin kinase B (TrkB)–Akt signaling pathway contribute to SCA6 pathophysiology (Cook et al., 2022), with both BDNF and TrkB expression reduced in the cerebellar vermis. This evidence concerns the gene NTRK2 and spinocerebellar ataxia type 6.