These results therefore show that increased β-arrestin1, as seen in brains of FTLD-tau and AD, strongly blocks the self-interaction of p62, an initial step required for p62-mediated clearance of cargo including misfolded tau (Babu et al, 2008; Itakura & Mizushima, 2011; Zheng et al, 2012; Wurzer et al, 2015). This evidence concerns the gene MAPT and Alzheimer disease.