The RNF182 is selectively upregulated in postmortem brains of AD patients, and the RNF182 overexpression triggers cell death of neurons.178 RNF182 physically interacts with ATPase 16 kDa proteolipid subunit (ATP6V0C), a key component of gap junctions and neurotransmitter release channels, and ubiquitinates ATP6V0C for proteasomal degradation. This evidence concerns the gene ATP6V0C and Alzheimer disease.