In agreement with these observations, the genetic silencing of STIM1 and Orai1 alleviated the increase in permeability induced by the pro-inflammatory mediator, High-Mobility Group Box 1 protein (HMGB1), in Ea.hy926 monolayers [181], whereas a selective siOrai1 alleviated tunicamycin-induced ER stress and unfolded protein response, which are a feature of atherosclerosis, were shown to be alleviated by a selective siOrai1 in HUVECs [182]. Here, ORAI1 is linked to atherosclerosis.