Under non-reducing conditions (i.e., in the absence of β-mercaptoethanol, β-ME), the levels of ATAD3A oligomers increased in immortalized mouse hippocampal HT-22 neurons and Neuro2a neuroblastoma cells exposed to oligomeric Aβ1–42 peptide in a time- and dose-dependent manner (Fig. 1a, Supplementary Fig. 2a), and in toxic Aβ-treated mouse primary cortical neurons (Fig. 1b). The gene discussed is ATAD3A; the disease is neuroblastoma.