SLC34A2 encodes a sodium-dependent phosphate cotransporter that actively transports inorganic phosphate into cells across epithelial membranes. The protein localizes to apical surfaces of specialized tissues including lung alveolar epithelium, intestinal epithelium, and renal proximal tubules, where it plays a critical role in phosphate homeostasis 1. Regulation of SLC34A2 occurs at transcriptional and post-translational levels in response to growth factors and hormonal signals, including epidermal growth factor in intestinal cells 2. Loss-of-function mutations in SLC34A2 cause pulmonary alveolar microlithiasis (PAM), a rare autosomal recessive disorder characterized by widespread calcium-phosphate crystal deposition in lung alveoli 3. Patients with PAM develop progressive dyspnea, hypoxemia, and potential respiratory failure; current management is supportive, with lung transplantation reserved for end-stage disease 4. In cancer contexts, SLC34A2 expression patterns differ by malignancy type. In non-small cell lung cancer and osteosarcoma, SLC34A2 is downregulated, and its restoration suppresses cell proliferation, migration, and invasion through PI3K/AKT pathway inhibition 5, 6. Conversely, SLC34A2 overexpression in ovarian cancer correlates with sensitivity to XPR1 inhibition, suggesting phosphate dysregulation as a therapeutic vulnerability 7. Lifastuzumab vedotin, an antibody-drug conjugate targeting SLC34A2, represents an emerging therapeutic approach in cancer.