We have previously reported that nemo-like kinase (Nlk) is a proline-directed serine/threonine kinase capable of interacting with and phosphorylating several neurodegenerative disease–causing proteins, namely, ataxin-1 and androgen receptor (AR), the proteins whose polyglutamine repeat expansion are causal for spinocerebellar ataxia type 1 (SCA1) and spinal and bulbar muscular atrophy (SBMA), respectively (7, 8). This evidence concerns the gene AR and spinocerebellar ataxia type 1.