When we studied myofibrils from the ACTC E361G transgenic mouse model of DCM, we found that the Ca2+ sensitivity of isometric force was not dependent on troponin I phosphorylation; likewise, there was no significant difference in kACT or kREL between natively phosphorylated and unphosphorylated myofibrils. Here, ACTC1 is linked to familial dilated cardiomyopathy.