In addition, Kristen T. Crowell and Charles H. Lang found that the reduction of 50 to 90% of thin filament (such as tropomyosin and a-sarcomeric actin), thick filament (myosin heavy and myosin light chains), Z-disk (a-actinin-3), and M-band (myomesin-2) proteins contributes to the intrinsic functional defects of muscle contraction during the sepsis recovery phase (34). The gene discussed is MYOM2; the disease is Sepsis.