YKT6 is a vesicular SNARE protein essential for membrane fusion and intracellular transport. Structurally, YKT6 functions as a v-SNARE mediating vesicle docking and fusion to specific cellular compartments 12. It participates in multiple transport pathways: endoplasmic reticulum to Golgi transport as part of SNARE complexes with GOSR1, GOSR2, and STX5; early/recycling endosome to trans-Golgi network transport with BET1L, GOSR1, and STX5; and autophagosome-lysosome fusion where it forms a priming complex with STX17 and SNAP29 23. YKT6 also possesses S-palmitoyl transferase activity and is essential for Golgi apparatus organization 45. Beyond canonical vesicular functions, YKT6 exhibits disease-relevant roles. In male fertility, YKT6 is indispensable for meiosis progression during spermatogenesis through vesicular transport regulation 6. In bladder cancer, YKT6 is significantly upregulated and promotes progression by stabilizing β-catenin through USP7-mediated deubiquitination, activating oncogenic Wnt/β-catenin signaling and epithelial-mesenchymal transition 7. Pan-cancer analysis reveals YKT6 upregulation in most tumors correlating with poor prognosis in multiple malignancies including lung adenocarcinoma, where elevated expression predicts adverse outcomes and YKT6 knockdown inhibits proliferation and migration 89. Additionally, YKT6 contributes to tumor-promoting metabolic reprogramming in pre-metastatic niches 10.