INTRODUCTION: STIM1 and STIM2 proteins are calcium sensors residing in the ER. They are involved in the regulation of SOCE (Store-Operated Calcium Entry) and take part in Ca2+ homeostasis and signaling. They participate in the regulation of numerous processes such as genes expression, neurotransmission, and neuronal morphology. STIM1 is also sensitive to redox state and may regulate functions of mitochondria. STIM2 is highly expressed in the neuronal tissue and was shown to be involved in processes leading to neurodegeneration. Oxidative stress and abnormal activity of mitochondria are frequently proposed to be a part of the mechanism that leads to the neurodegeneration. AIM(S): We aim to check the role of Stim2b zebrafish isoform in the activity of mitochondria, and its sensitivity to redox state. METHOD(S): Wild-type and stim2b‑/‑ zebrafish are being used in the experiments and oxidative stress is induced by 2 mM H2O2 treatment of 5dpflarvae. Thesefish lines express, specifically in neurons, a genetically encoded Ca2+ probe – GCaMP5G – that allows us to track changes in Ca2+ levels in response to oxidative stress. We use state‑of‑the‑art techniques of in vivo Ca2+ imaging using lightsheet microscopy and qPCR to analyze gene expression. RESULTS: We found that expression of genes (like catalase), that are known to be involved in response to the oxidative stress, was different in stim2b‑/‑ fish as compared to wild‑type in untreated larvae. mRNA level of catalase remains elevated in mutants also after oxidative stress induction. CONCLUSIONS: These data indicate that Stim2b might be involved in the brain response to oxidative stress. However, calcium imaging data, which are now being collected in vivo, are needed to confirm this hypothesis.