TFEB overexpression in models of Huntington's disease and spinal and bulbar muscular atrophy (SBMA, “Kennedy's Disease”) can increase autophagic clearance of polyQ‐expanded mutant huntingtin (mHtt; Sardiello et al, 2009; La Spada, 2012; Tsunemi et al, 2012) or androgen receptor (mAR; Cortes et al, 2014), limiting their accumulation into toxic aggregates. The gene discussed is AR; the disease is Kennedy disease.