In neurons from models of both Huntington's disease and Kennedy's disease, expanded polyQ tracts in mHtt (Yang et al, 2023) or mAR (Cortes et al, 2014) are able to bind and sequester the disordered Gln‐rich N‐terminus of TFEB, and disrupt its ability to upregulate the ATGs (Tsunemi et al, 2012), perhaps by impairing phase separation (Wang et al, 2022). The gene discussed is TFEB; the disease is juvenile Huntington disease.