SLC33A1 and early-onset autosomal dominant Alzheimer disease: Importantly, both haploinsufficiency of AT‐1 and biochemical inhibition of the ATases using compound 9 were able to rescue the Alzheimer's disease‐like phenotype in the mouse (Duran‐Aniotz, Cornejo, & Hetz, 2016; Peng et al., 2016).