Similarly, in both AD and in experimental model systems for AD an up-regulated miRNA-125b has also been found to down-regulate the expression of TREM2, IκBKG, SYN-2, 15-LOX, VDR and CFH that associate with deficits in phagocytosis, Aβ42 peptide clearance, NF-κB signaling, neurotrophism, deficits in the brain’s innate-immune response and an up-regulation of pro-inflammatory signaling (see below; Figure 2). The gene discussed is IKBKG; the disease is Alzheimer disease.