RAB3B is a small GTPase that functions as a key regulator of intracellular membrane trafficking, cycling between inactive GDP-bound and active GTP-bound states to recruit effector proteins responsible for vesicle formation, movement, tethering, and fusion 1. The protein is membrane-bound and interacts with Ca²⁺/calmodulin in a calcium-dependent manner 2, playing essential roles in trafficking cellular products from the endoplasmic reticulum through the Golgi apparatus to secretory vesicles, with high expression in brain and endocrine tissues 3. Rab3B has emerged as an oncogenic regulator across multiple cancer types. In glioma, elevated RAB3B expression correlates with tumor grade and promotes cell proliferation via cell cycle regulation, while silencing induces apoptosis through upregulation of pro-apoptotic proteins 4. In hypopharyngeal squamous cell carcinoma, RAB3B amplified from extrachromosomal circular DNA contributes to cisplatin resistance by inducing autophagy 5. In chordoma, RAB3B enhances mTORC1/S6 signaling and cell stemness; RAB3B/p-S6 status predicts mTORC1 inhibitor response 6. Pan-cancer analysis reveals RAB3B as an independent prognostic predictor correlating with tumor heterogeneity, immune microenvironment alterations, and DNA methylation changes across multiple malignancies 7. In cervical cancer, the circ_0000337/miR-155-5p/RAB3B axis promotes proliferation 8. Additionally, RAB3B dysregulation associates with long-term depression in suicide-related neurobiological pathology 9, suggesting broader neurological relevance beyond cancer.