AD-relevant stress-mediated increases in miRNA-34a in cultured brain cells, subsequent down-regulation in the expression of TREM2-3'-UTR reporter vectors, and rescue by anti-NF-kB or anti-miRNA-34a pharmacological strategies indicates that TREM2 and accessory genetic signaling components that drive defective Aβ42 peptide sensing and phagocytosis can be effectively quenched, at least in in vitro studies (Lukiw, 2013b; Zhao et al., 2013; Jones et al., 2014). The gene discussed is TREM2; the disease is Alzheimer disease.