SLC43A2 encodes a facilitated diffusion uniporter mediating stereospecific transport of L-phenylalanine, L-methionine, and branched-chain amino acids across cell membranes in a sodium-, chloride-, and pH-independent manner 1. The transporter functions in kidney and small intestine epithelial absorption 2 and at the blood-brain barrier 3. Clinically, SLC43A2 plays a critical immunosuppressive role in cancer. Tumor cells exploit high SLC43A2 expression to outcompete CD8+ T cells for methionine, depleting intracellular S-adenosylmethionine and reducing histone H3K79 dimethylation, thereby impairing T cell immunity and STAT5 expression 4. This mechanism extends to multiple malignancies: in esophageal squamous cell carcinoma, SLC43A2 participates in a feedback loop with NFκB signaling to suppress ferroptosis 5; in hepatocellular carcinoma, circPETH-147aa increases SLC43A2 mRNA stability to drive methionine deficiency in T cells 6; and in acute myeloid leukemia, SLC43A2 correlates with T cell exhaustion markers and poor survival 7. YAP-mediated transcriptional activation of SLC43A2 creates a positive feedback loop promoting anticancer drug resistance 8. In pancreatic ductal adenocarcinoma, VIRMA-mediated m6A modifications decrease SLC43A2 levels, reducing phenylalanine absorption and oxidative stress to promote tumor progression 9. SLC43A2 represents a promising therapeutic target for enhancing immunotherapy and overcoming metabolic immune evasion.