In fact, several manuscripts pointed toward some role of SST in the etiology of AD by documenting that (i) SST-releasing neurons are often observed in spatial proximity to plaques13, (ii) levels of SST receptors are reduced in AD14, (iii) SST expression levels decline with age, and even more pronouncedly in AD, (iv) binding of SST to its receptors triggers a signaling cascade, which controls the release of proteolytic enzymes involved in the degradation of Aβ15, and (v) genetic variants within the SST gene locus alter the risk for AD16,17. The gene discussed is SST; the disease is Alzheimer disease.