Patch clamp studies in the early eighties revealed the existence of a voltage-gated K+(Kv) channel in human lymphocytes that resembled delayed rectifier K+ channels in electrically excitable cells (DeCoursey et al., 1984; Matteson and Deutsch, 1984; Cahalan et al., 1985; Schlichter et al., 1986). Classical neuronal K+ channel blockers (4-aminopyridine, tetraethylammonium and quinine) and classical calcium channel blockers (verapamil, diltiazem and nifedipine) blocked this channel at micromolar to millimolar concentrations (Chandy et al., 1984; DeCoursey et al., 1984; Sabath et al., 1986). Despite having widely differing structures, these compounds inhibited cytokine production and T-cell proliferation with a potency parallel to channel block. The fact that these agents were not cytotoxic, acted reversibly, inhibited only if administered within the first 24 h, and did not suppress expression of IL-2 receptors or proliferation by exogenous IL-2, led us to postulate that K+ channels are required for an early phase of T-cell activation (Chandy et al., 1984). These results suggested that clinically useful immunosuppressants might be developed by selectively targeting lymphocyte K+ channels, an idea made highly attractive by the excellent track record of channel blockers in the therapeutic management of stroke, epilepsy and cardiac arrhythmias.