SLC6A12 encodes a sodium- and chloride-dependent transporter that mediates cellular uptake of GABA and betaine 1. The transporter plays critical roles in GABAergic neurotransmission through GABA reuptake into presynaptic terminals and in osmotic regulation 1. In cancer biology, SLC6A12 demonstrates significant pathological relevance. In hepatocellular carcinoma, SLC6A12 transports GABA, which directly stabilizes β-catenin and activates Wnt/β-catenin signaling, promoting metastasis 2. In ovarian cancer, aberrant hypomethylation of the SLC6A12 promoter increases expression 8.1-14.0-fold in metastases, enhancing cell migration and invasion 3. Downregulated lncRNAs regulate SLC6A12 expression in cholangiocarcinoma through transcription factor recruitment 4. SLC6A12 also contributes to neuroinflammatory and autoimmune diseases. In rheumatoid arthritis, high salt promotes macrophage pyroptosis through SLC6A12-mediated sodium transport and SGK1/p38 MAPK/NF-κB signaling activation 5. In Parkinson's disease, elevated SLC6A12 expression promotes neuronal injury via MAPK signaling 6. A genetic polymorphism (rs216250) associates with negative symptoms in schizophrenia 7, and SLC6A12 variants are implicated in aspirin-exacerbated respiratory disease 8. These findings position SLC6A12 as a multifunctional transporter with therapeutic potential across cancer, neurological, and inflammatory diseases.