Adipose tissue has a specialized role in energy storage and thermogenesis. However, when there is excess lipids over the storage capacity of adipose tissue, excess lipids “spill over” may occur from adipose to non-adipose tissues. Abnormal lipid accumulation in non-adipose tissues such as skeletal muscle and liver, not in WAT, is known to cause lipotoxicity : endoplasmic reticulum stress, increased inflammation response, mitochondrial dysfunction, insulin resistance (IR) and other effects. Therefore, profer regulation of adipogenesis is important for the homeostasis of lipid metabolism. There was several studies that relates SOCE and adipogenesis. However, the detailed mechanism of SOCE on the regulation of adipogenesis remains elusive. In this study, we show STIM2β expression level is increased during adipogenesis and functions as a regulator of adipogenesis. STIM2β KO 3T3-L1 cell line showed increased lipid accumulation during adipogenesis in comparison with WT cell line. STIM2β KO affects to Ca2+ signaling on 3T3-L1 cell and leads change in cell cycle. STIM2β KO mouse showed difference in adipose tissue development in comparison with WT. Our data provide an insight on the importance of intracellular Ca2+ concentration regulation by STIM2β on adipose tissue development.