SLC38A4 encodes a sodium-dependent symporter that transports neutral amino acids across the cell membrane, preferentially moving smaller amino acids such as glycine, alanine, serine, asparagine, and threonine. The transport process is electrogenic and pH-dependent, with partial tolerance for lithium substitution of sodium. SLC38A4 plays important roles in metabolic regulation and fetal development. Genetic variants in SLC38A4 are associated with glucose metabolism: the 292 C>T polymorphism showed significant association with elevated glucose levels in normal weight full-term healthy newborns 1, while the 1304 G>A variant was associated with hyperglycaemia in a broader cohort and remained significant after adjustment for body mass index, waist circumference, and triglycerides 2. SLC38A4 expression is dysregulated in disease contexts: reduced expression occurs in early preterm intrauterine growth restriction placentas 3, and increased SLC38A4 expression correlates with abnormal fetal birth weight, particularly in fetal macrosomia 4. In hepatocellular carcinoma, SLC38A4 functions as a tumour suppressor through modulation of the Wnt/β-catenin/MYC/HMGCS2 axis, with low expression associated with poor prognosis 5. Additionally, SLC38A4 expression increases in pancreatic α-cells under conditions of disrupted glucagon receptor signaling 6, and in diabetes, elevated SLC38A4 expression contributes to amino acid accumulation that drives mTORC1-mediated hyperglucagonaemia 7. A lung cancer association study identified the SLC38A4 rs2429467 C>T variant as protective against non-small cell lung cancer 8.