“…Critically, the absence of any A17 hDEG in MADAD may also reflect low sensitivity of MADAD itself to detect subtle transcriptional change in human AD, because failure to detect low-expression genes on whole-tissue microarrays would carry through the meta-analysis approach. Indeed, the human orthologs of several nonoverlapping A17 hDEGs, including filaggrin (FLG), inflammasome regulator NLRP10 (NLRP10), putative antioxidant CCDC80 (CCDC80), and IL-2 receptor alpha (IL2RA), were missing from MADAD but have been implicated in human AD genome-wide association studies (Paternoster et al, 2015) and other work (Elias et al, 2017;Furue et al, 1994;Miyai et al, 2016).…”