Due to reported nonspecific effects of TRAM‐34 and other compounds modulating SK4 (Agarwal et al., 2013; Wulff et al., 2000), proof‐of‐concept studies are required to establish the oncogenic roles of endogenous SK4 channels for Ca2+ signalling and proliferation and thereby their therapeutic potential in breast cancer. This evidence concerns the gene KCNN4 and breast cancer.