Disruption of this calmodulation appears to be a prominent driver of arrhythmia, as observed through LQTS‐associated Kv7.1 mutations which disrupt CaM interactions at the channel C‐terminus (Ghosh et al., 2006; Gonzalez‐Garrido et al., 2021; Mousavi Nik et al., 2015; Sachyani et al., 2014; Schmitt et al., 2007; Shamgar et al., 2006; Tobelaim et al., 2017; Yang et al., 2009; Zhou et al., 2016). This evidence concerns the gene CALM1 and familial long QT syndrome.