Although the loss of body weight and muscle atrophy in chronic lung disease is a multifactorial event, these accumulating data suggest that both mIL-6 and mIL-33 are increased in serum during lung fibrosis, which may synergistically cause body weight loss in mice through the activation of STAT3 and AMPK signaling to induce the expression of proteolysis- and lipolysis-related genes. Here, STAT3 is linked to pulmonary fibrosis.