YKT6 is a vesicular SNARE protein that mediates vesicle docking and fusion, functioning in endoplasmic reticulum-to-Golgi transport as part of a SNARE complex with GOSR1, GOSR2, and STX5, and in early/recycling endosome-to-trans-Golgi network transport with BET1L, GOSR1, and STX5. YKT6 possesses S-palmitoyl transferase activity and is essential for the structural and functional organization of the Golgi apparatus 1. Beyond classical trafficking, YKT6 forms a priming complex with STX17 and SNAP29 on autophagosomes, facilitating autophagosome-lysosome fusion and autophagy flux 2. In cancer contexts, YKT6 exhibits oncogenic functions distinct from its housekeeping role. YKT6 is significantly upregulated in multiple tumor types, including bladder cancer, lung adenocarcinoma, and head and neck squamous cell carcinoma, where elevated expression correlates with poor prognosis 34. In bladder cancer, YKT6 promotes cell proliferation, migration, and metastasis by activating Wnt/β-catenin signaling through USP7-mediated deubiquitination of β-catenin 5. In estrogen receptor-positive breast cancer, YKT6 regulates cell surface levels of the leucine transporter SLC7A5, promoting nutrient uptake and resistance to endocrine therapy 6. Additionally, in non-small-cell lung cancer, YKT6 expression in primary tumors correlates with macrophage infiltration and immunosuppression in pre-metastatic niches 7. These findings position YKT6 as both a fundamental membrane-trafficking protein and an emerging therapeutic target in cancer.