The increase in CF KATP expression, and functionality within the border region of an infarct scar, was postulated to contribute towards CF electrophysiological signalling in rat hearts; which occurred in response to reinfarction (the reoccurrence of symptoms of ischemia in patients or animals with a previous diagnosis of MI), and may have decreased the depolarising effect enacted on CM by CF [265]. This evidence concerns the gene CFTR and myocardial infarction.