Aβ peptides accumulate both on and inside mitochondria in AD, impairing protein import through TOM complex blockade and directly inducing mitochondrial dysfunction linked to cognitive decline, though Aβ1‐42 and TOM complex binding alone suffice to inhibit import.[67, 68] Our data reveal that exposure to the Aβ1‐42 peptide suppresses the overall expression of SENP6, consequently augmenting TOM40 SUMOylation (Figure 6C–E). The gene discussed is PRPF6; the disease is Alzheimer disease.