Consistent with reduced autophagic function associated with aging and inflammation (12), we observed that HTT levels decline with age in the striatum and cortex, tissues that degenerate in HD, and that the proinflammatory kinase IKKbeta may activate HTT’s autophagic function through phosphorylation of HTT serine 13 in vivo (8, 13, 14). This evidence concerns the gene HTT and Huntington disease.