Receptor-mediated activation of leukocytes by inflammatory stimuli elicits Ca2+ ion influx as a common and important activation mechanism that has been well established in the literature for over a decade. Inhibiting such receptor-operated Ca2+ influx channels is a potentially attractive strategy for developing anti-inflammatory drugs to attenuate leukocyte activation. Until very recently, the molecular identity of these channels has been unknown, which has hampered drug development in this area. However, the recent explosion of molecular information about one particular family of non-voltage-activated Ca2+ channels, the transient receptor potential (TRP) channels, together with emerging knowledge of their distribution, function and regulation, suggests that they represent a key subgroup of these channels and are therefore potentially attractive drug targets.