Knockdown of S100A9 significantly attenuated the increase of Ca2+ levels provoked by C-terminals of APP or by Aβ treatment (Ha et al., 2010); however, others observed that a reduction of S100A9 extracellular release is followed by an increase in intracellular Ca2+ levels (Lee et al., 2013), evidencing a correlation between S100A9 and calcium dysregulation in AD. Here, S100A9 is linked to Alzheimer disease.