Inorganic phosphate (P i ) is a constituent of important biological molecules (e.g., nucleic acids and phospholipids) and is essential for cellular energetics and signaling, and protein synthesis as well as skeletal development in all mammalian organisms. Inadequate P i supply causes bone malformations such as rickets and spinal deformations, whereas an excess in P i is linked to vascular calcification or ectopic CaP i deposits. In general, whole-body P i homeostasis is maintained by transepithelial transport mechanisms in the small intestine and kidney where P i is absorbed from the diet and reabsorbed from the glomerular filtrate, respectively. The renal proximal tubule is the main locus of P i regulation so that under Bsteady-state^physiological conditions, renal P i -excretion corresponds approximately to dietary P i intake.Membrane transport proteins belonging to the SLC34 solute carrier family 1 lie at the heart of maintaining P i homeostasis. In the small intestine, NaPi-IIb (SLC34A2) mediates luminal P i uptake together with a paracellular component, whereas the renal isoforms NaPi-IIa (SLC34A1) and NaPi-IIc (SLC34A3) are responsible for P i reabsorption in the proximal tubule. This Special Issue focusing on phosphate transport mediated by SLC34 proteins was conceived to coincide with an important milestone in renal physiology: the expression cloning of the first member of the SLC34 family (NaPi-IIa) just over a quarter of a century ago [33]. This, together with the subsequent identification of the other two SLC34 isoforms [24,42], has paved the way for a deeper understanding of the molecular basis of P i homeostasis, many aspects of which are the subject of dedicated reviews in this issue. Whereas the pivotal role of SLC34 cotransporters in maintaining P i homeostasis is undisputed, other carriers such as PIT-1 and PIT-2 (SLC20 family) may also contribute to epithelial transport of P i in the intestine and the kidney. However, their respective contributions to 1 Historically, the nomenclature of the cloned, mammalian P i transporters followed a strictly chronological convention, beginning with the type 1 (NaPi-I) [10,53] (since shown to be related to an anion conductance and not directly mediate Na-dependent P i transport [8]); the type II (NaPi-II [33] or npt2) and the type III (NaPi-III [28,29], or Pit-1,2). The widely used solute carrier (SLC) nomenclature [22] assigns the type I transporters to the SLC17 gene family; type II Na-P i transporters to SLC34 and type III transporters to SLC20, respectively. The SLC system is increasingly used, i.e., SLC34A1, SLC34A2, and SLC34A3 for the human type II transporters NaPi-IIa, NaPi-IIb, and NaPi-IIc, respectively. The structurally similar isoforms are grouped into the same sub-family (SLC34A) with individual indices (1, 2, 3). This nomenclature is easily applicable to most vertebrates; it only becomes less clear in the case of fish that have undergone genome duplications followed by lineage specific gene losses.