Recently, a study trying to evaluate whether activation of RhoA/ROCK pathway could be involved in mitochondrial dysfunction induced by endotoxemia demonstrated that RhoA/ROCK inhibition normalized mitochondrial respiration in LPS heart and reduced proinflammatory and oxidative stress responses, cytoskeleton disorganization, and mitochondrial ultrastructural damage. This evidence concerns the gene RHOA and serum lipopolysaccharide activity.