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121 OleaN.PulgarR.PerezP.OleaSerranoF.RivasA.NovilloFertrellA.et al (1996)

According to the model we have previously described, K ATP current activation driven by mitochondrial instability induces lability in the cellular action potential duration and alters the refractory period, which increases the dispersion of repolarization in the tissue and promotes reentrant arrhythmias through the formation of metabolic sinks [6, 7]

The enzyme's role in DNA repair mechanisms also implicates it in the response to genomic stress and the prevention of mutations that could lead to malignancies