Monocyte inflammatory products released during sepsis, especially TNFα, have been shown to impair skeletal muscle contractility through an increase in mitochondrial or cytosolic production of reactive oxygen species (ROS) [18], and calcium-activated calpains lead to Z disk disruption and release of myofilaments, a phenomenon that has been shown to be up regulated in sepsis [18]. The gene discussed is TNF; the disease is Sepsis.