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NCC, a thiazide-sensitive NaCl co-transporter, is found on the apical membrane of the distal convoluted tubule, where it is the principal mediator of Na+ and Cl- reabsorption in this segment of the nephron. It is activated by phosphorylation, and has been implicated in renal NaCl and K+ homeostasis (1). Regulation of NCC expression and phosphorylation by dietary NACl restriction appears to involve SGK1(1). In experiments with angiotensin II-infused mice, increased sensitivity to Ang II may involved over-activity of NCC (2). Therefore, NCC is the target of thiazide diuretics used in the treatment of hypertension (1). Molecular experiments have also shown that NCC has been detected in the lens cortex, core and fiber cells of a rat (3).