Previous studies showed that the Ca2+ gated K+ channel KCa3.1 can play an important role in the progression of different cancer types like the Pancreatic Duct Adenocarcinoma (PDAC) and that the KCa3.1 blocker Clotrimazole decreases the proliferation of the PDAC line MiaPaCa-2 but not Panc-1, in which the channel is poorly expressed (Jäger, 2003, 10.1124/mol.65.3.6309). However, Clotrimazole also inhibits cytochrome P450; thus, proliferation might be influenced by this side effect. Nevertheless, studies in which KCa3.1 was silenced suggested that the channel is important for MiaPaCa-2 cell proliferation and migration (Bonito, 2016, 10.1007/s00424-016-1891-9). We are currently investigating the role of KCa3.1 in melanoma cell lines, checking if channel blockage alone can impact cell growth also in this type of cancer. To this purpose, we use two different channel blockers: the already mentioned Clotrimazole and Senicapoc, a more KCa3.1-selective blocker (Staal, 2017, 10.1007/s11064-017-2223-y). In order to better discriminate between unspecific toxicity and effects strictly correlated to channel blockage, we performed patch-clamp experiments and MTT viability assays on the melanoma line WM266 and on Panc-1, used as negative control. We found that Panc-1 cells, as expected, do not exhibit Ca2+-activated KCa3.1 currents, while such currents were present in WM266, where they were blocked by both Clotrimazole and Senicapoc. To test how channel blockage can impact cell proliferation, we performed MTT viability assays, which showed that Senicapoc affects the growth not only of WM266 but also, at a similar extent, of Panc-1, which lack KCa3.1 currents. This raises the question of whether Senicapoc can impact melanoma cells growth only by blocking the channel. To answer this question, we will perform further experiments (including migration assays) and we will present our newest data. Supported by AIRC and PRIN.