Accumulating evidence suggest that a deregulation of calcium signalling may play a major role in Alzheimer’s disease progression; CaBPS such as parvalbumin, calbindin and calretinin are upregulated in the hippocampus of 3-month-old APPswe/PS1dE9 transgenic mice, possibly to control cellular homoeostasis and synaptic plasticity, but losing cellular capacity to pathophysiological processes by the age of 12 months (Verdaguer et al. 2015). The gene discussed is CALB1; the disease is Alzheimer disease.