Tat-BECN1 triggers degradation of amyloid fibrils in Alzheimer’s disease (Luo et al., 2018) and middle-aged (De Risi et al., 2020) brains and rescues memory deficits, removes ubiquitinated protein aggregates induced by WNV infection (Kobayashi et al., 2020), relieves abnormal cytosolic and nuclear glycogen storage in liver with distal urea cycle disorders (Soria et al., 2021), clears glaucoma-causing mutant myocilin and reduces elevated intraocular pressure (Kasetti et al., 2021), enhances FAM134B-mediated ER-phagy of misfolded procollagen in chondrocytes (Forrester et al., 2019). Here, BECN1 is linked to early-onset autosomal dominant Alzheimer disease.