Multiple previous studies have reported abnormal plasma levels of EGF in AD patients, [120–122] and two recent studies on EGF have demonstrated its protective effects on AD by preventing amyloid-beta (Aβ)-induced angiogenesis deficit to brain endothelial cells in vitro and in vivo.[123,124] Recent studies have also described that the EGFR internalization after EGF binding was strongly inhibited when ANKRD13 proteins were over-expressed.[118] This mechanism implicates a potential regulatory effect of the ANKRD13 family on AD pathology through the regulation of internalization of EGFR. The gene discussed is EGFR; the disease is Alzheimer disease.