Arrell et al. (2001) and Morano et al. (1996) showed that a small amount of ALC1 appeared in the ventricles of adult people with chronic cardiovascular disease and hypertrophic, dilated cardiomyopathy, similarly to our I/R mechanism, which increased the maximal shortening velocity, rate of tension redevelopment, and isometric force generation [17,20]. The gene discussed is MYL4; the disease is dilated cardiomyopathy.