PGs upregulate cell signaling proteins (e.g., tumor necrosis factor alpha (TNF-α)) and muscle degradation pathways (chronic inflammation) and suppress cell growth factors such as insulin-like growth factor-1 (IGF-1), which, in turn, causes greater skeletal tissue damage, enhancing the progression of DMD and ultimately muscle fibrosis [10,13]. The gene discussed is IGF1; the disease is Duchenne muscular dystrophy.