To gain further insight into how the CaM E105A mutation leads to severe cardiac arrhythmia and determine quantitatively how this specific mutation alters the association of CaM with RyR2 leading to diminished inhibition, we initially bacterially expressed and purified large quantities of recombinant CaMWT and CaME105A proteins, as we have previously described [37]. The gene discussed is CALM1; the disease is cardiac arrhythmia.