Finally, we show that BIN1iso1 endosomal defects and toxicity can be attenuated by a gain of function of Rab11, which dovetails with data showing a colocalization of BIN1 with Rab11 [56] and indicating that Rab11 activity is altered in AD in relationship with endosomal trafficking [5, 63, 66]. Here, RAB11A is linked to Alzheimer disease.