SLC4A11 is a multifunctional transmembrane transporter primarily known for its critical role in corneal endothelial function and cellular metabolism. The protein functions as an electrogenic H+ transporter activated by NH3 and alkaline pH, facilitating ammonia transport across cellular membranes 1. In hepatocellular carcinoma, SLC4A11 acts as an ammonia transporter that promotes cancer cell survival by enabling ammonia excretion and supporting cancer stemness through ammonia import for biosynthesis 23. The transporter plays a crucial role in mitochondrial function by providing ammonia-sensitive H+ uncoupling that reduces glutamine-driven mitochondrial membrane potential hyperpolarization and suppresses superoxide production 1. Mutations in SLC4A11 cause congenital hereditary endothelial dystrophy (CHED) and Fuchs endothelial corneal dystrophy, characterized by corneal edema and endothelial dysfunction 45. Disease pathogenesis involves energy shortage due to reduced ATP production and mitochondrial dysfunction, leading to insufficient energy for the Na+/K+-ATPase pump essential for corneal transparency 6. The predominant variant in human corneal endothelium is variant 2 starting at methionine 36 7. SLC4A11 expression is regulated by oxidative stress through the NRF2 transcription factor 1.