Our findings support a notion that enhanced LC3-II activation/accumulation associated with unchanged p62, inconsistent recruitment of PINK1/Parkin to mitochondria and elevated levels of mitochondrial proteins could be attributed to both induction of basal autophagy and defective clearance of autophagic substrates due to increased mitochondrial stress or dysfunction in AD neurons. The gene discussed is SQSTM1; the disease is Alzheimer disease.