Synaptotagmin 4 (Syt4) is a calcium-sensing synaptic vesicle protein. It is involved in processes such as the release of neurotransmitters and neurotrophic factors, and is associated with pathways like calcium signaling [3,4]. Syt4 has significance in various biological aspects including cell maturation, exosomal secretion, and may be related to neurodegenerative and neurodevelopmental diseases [2,5].

In prostate cancer, down-regulation of Syt4 combined with enzalutamide enhanced the antiproliferative effect on resistant cells. Syt4 promotes vesicle efflux by binding to SNAP25, contributing to enzalutamide resistance [1].

In gastric cancer, Syt4 was higher in tissues, and its elevation correlated with adverse prognosis. Functionally, it promoted tumorigenesis via a Ca2 +-dependent MAPK mechanism, and amlodipine could attenuate its effects [3].

In pancreatic β-cells, Syt4 ablation increased basal insulin secretion and compromised glucose-stimulated insulin secretion, while precocious expression also impaired islet functions [5].

In the context of chronic stress, Syt4 overexpression in the medial prefrontal cortex was pro-susceptible to anhedonia, while knockdown was pro-resilient, with the effects mediated through BDNF-TrkB signaling [4].

In summary, Syt4 plays crucial roles in multiple biological processes. Its dysregulation is associated with various diseases including prostate, gastric cancers, and may impact mental health related to stress-induced anhedonia. The study of Syt4 through gene-manipulation models has provided insights into its functions in these disease-relevant contexts.