Lee et al. (2016) demonstrated in vitro that Aβ triggers a TRPA1-dependent Ca2+ influx and astrocytic activation. Additionally, ablation of TRPA1 in APP/PS1 transgenic mice slowed the progression of AD and improved learning and memory performance, and reduced Aβ plaques and cytokines (Lee et al., 2016). These results have been further supported by TRPA1 expression in HEK cells, where Aβ is also capable of inducing TRPA1 dependent Ca2+ signaling, that activate transcription factors such as NF-κB and NFAT and promote expression of pro-inflammatory cytokines (Lee et al., 2016). The gene discussed is TRPA1; the disease is Alzheimer disease.