To verify that NRBF2 deletion also promotes the buildup of human insoluble Aβ42, we crossed NRBF2-KO mice with 5XFAD mouse model — a well characterized AD model known to overproduce Aβ42 [47] — and found that NRBF2-KO mice carrying 5XFAD hemizygous allele contained enhanced levels of insoluble Aβ42 in the hippocampus compared to controls (Additional file 2: Figure S5D), further supporting that NRBF2 deficiency accelerates the aggregation of insoluble Aβ42 in the hippocampus. The gene discussed is NRBF2; the disease is Alzheimer disease.