Several studies evidenced a strong positive correlation between S100A9 levels and AD pathology: knockdown of S100A9 improved cognition on model mice of AD and reduced global levels of Aβ and APP C-terminal fragments due to decreased activity of the beta-site amyloid precursor protein cleaving enzyme 1 (BACE-1) (Chang et al., 2012). The gene discussed is APP; the disease is Alzheimer disease.