The question arises as to whether in AD/CMRD and for the case of SAR1, for which there are also two human paralogues, the disease becomes manifest only in tissues in which there is insufficient amounts of the second paralogue to compensate for the loss of activity of the first paralogue or whether a specific cargo (chylomicrons) is strictly dependent on a specific paralogue(s) of the secretion machinery. This evidence concerns the gene SAR1A and Alzheimer disease.