Petit A, Knabe L, Khelloufi K, et al. - Researchers analyzed air–liquid interface–reconstituted bronchial epithelium from controls as well as from smokers (with and without COPD) to study calcium (Ca2⁺) signaling. They investigated how smoking impaired Ca2⁺ signaling. In patients with COPD, a reduction was noted in the endoplasmic reticulum (ER) depletion of Ca2⁺ stores. In epithelial cells from smokers (regardless of COPD status), they noted a reduction in Ca2⁺ influx. Additionally, a reduction in ER Ca2⁺ release was induced by acute cigarette smoke (CS) exposure, which was significant in smokers. Acute CS exposure resulted in a reduction in Ca2⁺ influx only in controls. Findings are indicative of impaired Ca2⁺ signaling in smoker epithelia (irrespective of COPD status) as well as the involvement of ORAI3 in Ca2⁺ signaling. An additional implication of ORAI3 in ciliary beating was also shown.