Passive K+ transport in human erythrocytes (defined as ouabain-insensitive transport) was inhibited 70% by replacement of Cl- by several permeant monovalent anions. The Vmax of Cl--dependent K+ influx was 1.14 mmol . liter-1, hr-1; its apparent Km for K+ was 4.7 mM. There was a much smaller component of Na+ influx dependent on Cl- (Vmax, 0.23 mmol . liter-1 . hr-1). Furosemide and other inhibitors of Cl- transport inhibited passive K+ transport to the same extent as replacement of Cl-, but 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, a specific inhibitor of anion exchange in erythrocytes, was ineffective. The Cl--dependent K+ transport, which may be K+/Cl- cotransport, could reflect a mechanism for regulating cell volume.