Again, this is at odds with the findings in short-term expression models used in Davis et al. (9), where Ca2+ transients returned to baseline more quickly when the myofilament was directly desensitized and suggests that DCM mutations in the thin filament, which are spatially remote from the regulatory binding site of TnC, drive disease pathogenesis in a mechanistically more complex manner than first thought. The gene discussed is TNC; the disease is familial dilated cardiomyopathy.