These results demonstrate the impact of decreased parkin solubility (Lonskaya et al, 2012b; Lonskaya et al, 2013), which co-localizes with intraneuronal Aβ1–42 in post-mortem AD brains (Lonskaya et al, 2012c), suggesting failure to facilitate amyloid clearance. The gene discussed is PRKN; the disease is Alzheimer disease.