Insulin is secreted from pancreatic beta cells in response to glucose stimulation via regulated exocytosis. The exocytosis of insulin granules is triggered upon increase in cytosolic calcium concentration and can be further amplified by cAMP [1]. How does cAMP amplify glucose-induced insulin secretion? General consensus is that cAMP augments insulin secretion by acting through PKA- and Epac2-dependent pathways, but precise mechanism is not fully understood [2, 3]. It was previously suggested that one of the many roles of cAMP is the enhancement of calcium signals either by voltage-dependent calcium entry or intracellular calcium mobilization [4]. To determine the role of cAMP in calcium dynamics we used forskolin which increases the cytosolic cAMP concentration through the activation of adenylate cyclase. Oregon Green 488 BAPTA-1 AM (OGB-1) calcium dye was used to record oscillatory changes in cytosolic calcium concentration in mouse pancreas tissue slices using confocal laser scanning fluorescence imaging. In the absence of forskolin the sub-stimulatory glucose concentration failed to increase cytosolic calcium concentration in beta cells while the stimulatory glucose concentration caused stable fast calcium oscillations (3-6/min) on a sustained plateau phase. Addition of 10 μM forskolin in the extracellular solution triggered high frequency calcium oscillations (3-6/min) even at otherwise sub-stimulatory glucose concentration. The effect on calcium oscillations was belated, triggered several minutes after the addition of forskolin. When the same concentration of forskolin was added to the extracellular solution together with the stimulatory glucose concentration, the frequency of calcium oscillations almost doubled (6-12/min) compared to glucose stimulus only. Again, the effect of forskolin was observed after several minutes. To determine which of the two cAMP dependent pathways was responsible for augmented calcium oscillations in pancreatic beta cells, we performed the same sets of experiments on the pancreatic slices from mice lacking the Epac2 protein. Most probably Epac2 is not crucial for cAMP-augmented cytosolic calcium oscillations in mouse pancreatic beta cells since forskolin triggered calcium oscillations at sub-stimulatory glucose concentration also in the Epac2 KO mice. Furthermore, at stimulatory glucose concentration the frequency of calcium oscillations was increased after addition of forskolin. These results corroborate previously published data describing that phosphorylation of several targets by PKA is responsible for cAMP augmented calcium oscillations in pancreatic beta cells [5].