Yet TRESK is strongly upregulated in several leukemic cell lines as well as in patients with T-ALL [197]. In vivo real time K+ flux measurements and concurrent patch-clamp data on Jurkat cells revealed that both TRESK and Kv1.3 mediate AVD in the intrinsic apoptosis pathway, yet TRESK is transiently upregulated by apoptotic stimulus (staurosporine) and then completely inactivated in a half of hour, causing a strong membrane depolarization, whereas the Kv1.3 contribution to the K+ efflux was more constant in time [147]. This evidence concerns the gene KCNA3 and acute lymphoblastic leukemia.