SLC12A7 encodes a potassium-chloride cotransporter that mediates electroneutral K-Cl cotransport activated by cell swelling. It plays a critical role in inner ear physiology, where it promotes K+ uptake into cochlear supporting cells and contributes to K+ recycling essential for survival of hair cells and maintenance of the organ of Corti. The transporter may also contribute to basolateral Cl− extrusion and renal acidification. SLC12A7 variants cause both autosomal dominant and recessive nonsyndromic hearing loss, reflecting its essential function in cochlear ion homeostasis. Beyond auditory disease, recent evidence identifies SLC12A7 dysregulation in multiple malignancies. In adrenocortical carcinoma (ACC), SLC12A7 gene amplification occurs in 65–68% of cases and correlates with increased expression and non-functional tumors 1. SLC12A7 overexpression promotes ACC cell motility and invasive capacity, potentially through alterations in osmotic stress, bone morphogenetic protein, and Hippo signaling 2. Pan-cancer analysis shows SLC12A7 upregulation correlates with unfavorable outcomes and altered immune infiltration, with functional assays confirming its role in hepatocellular carcinoma cell proliferation, migration, and invasion 3. SLC12A7 amplification has also been documented in HER2-negative gastric cancer 4 and identified as a potential biomarker for erlotinib resistance 5. These findings establish SLC12A7 as both a regulator of normal ion transport and an emerging oncogenic driver across cancer types.