Owing to its remarkable benefits on metabolic health and its demonstrated presence in adult humans, beige or ‘brite’ adipocytes hold great promise to combat obesity and metabolic diseases. Delineation of the mechanisms involved in adipocyte ‘beiging’ or ‘browning’ is thus of particular interest. Previous studies of the molecular regulatory pathways that drive the beiging of white adipose tissue (WAT) have centered on the cyclic adenosine monophosphate (cAMP)-related signaling (Wang and Seale, 2016; Cohen and Kajimura, 2021). Acting via the cAMP–protein kinase A pathway, norepinephrine dually stimulates adipocyte lipolysis and the expression of thermogenic genes, such as uncoupling protein 1 (Ucp1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (Ppargc1a) (Inagaki et al., 2016). While the second messenger calcium (Ca2+) is fundamental to a wide variety of cellular processes including, but not limited to, muscle contraction, gene transcription, exocytosis, and cellular metabolism in virtually all eukaryotic cells (Arruda and Hotamisligil, 2015), whether and how Ca2+ signals orchestrate WAT beiging remains largely unclear, in part because of a limited understanding of the regulatory mechanism that controls intracellular Ca2+ dynamics in adipocytes.