Another study showed that overexpression of the human amyloid precursor protein (APP) with the familial Swedish mutation (APPswe) in a mouse neuroblastoma cell line (N2A) altered the structure and function of mitochondria-associated membranes, mitochondrial dynamics, biogenesis and protein import as well as the stress response (Fernandes et al., 2021). The gene discussed is APP; the disease is neuroblastoma.