Insulin secretion from pancreatic beta cells occurs in response to depolarisation-induced calcium ion (Ca2+) influx. Mitochondria are an important regulator of intracellular Ca2+ concentration as they can sequester Ca2+ and thus buffer fluctuations of Ca2+ within cells. Olof Idevall-Hagren and co-workers (Griesche et al., 2019) now investigate the effect of subcellular mitochondrial localisation on insulin secretion. Their analysis shows that the cell cortex is enriched in mitochondria; however, upon depolarisation, mitochondria leave the cortical region. Interestingly, depolarisation, and the resulting cellular Ca2+ influx, induce the accumulation of cortical actin. Using an optogenetic experimental setup that allows the authors to forcibly relocate mitochondria to the cortex, they demonstrate that the inhibition of actin polymerisation with latrunculin A prevents the optogenetically induced mitochondrial relocalisation to the cortex. This suggests that actin is required for mitochondrial retention near the plasma membrane. To elucidate the role of cortical mitochondria in insulin secretion, the authors show that forced mitochondrial relocalisation to the plasma membrane promotes Ca2+ sequestration and decreases cellular responses to Ca2+ influx. Critically, they also notice a decrease in diacylglycerol spikes, which are a proxy for insulin secretion, at the plasma membrane when mitochondria are forcibly redistributed to the cell cortex. Thus, this study suggests that the subcellular localisation of mitochondria is a newly discovered regulator of insulin secretion from beta cells.