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The cover illustration shows the poor tolerance of K_ATP channel-knockout mice (white) in response to haemodynamic load compared to wildtype counterparts (black). Genetic deletion of the Kir6.2 channel pore precipitated heart failure with anasarca, terminal bradycardia, and cardiomegaly associated with nuclear up-regulation of pro-remodeling pathways. See Yamada et al. 1053 , and accompanying Perspective (on p.767 ) highlighting the new role of K_ATP channels in protecting against congestive heart failure.