Studies have shown that factors such as malnutrition, chronic low-grade inflammation, and reduced physical activity in the context of sarcopenia may further inhibit the synthesis and secretion of IGF-1 in the liver and muscles (23); in local tissues, hydrolytic cleavage of IGF-binding proteins (IGFBPs) is a key step in releasing free IGF-1 and regulating its bioavailability (24), but this regulatory process may be disrupted in the pathological microenvironment of sarcopenia, thereby inhibiting IGF-1 signaling (25). The gene discussed is IGF1; the disease is nutritional deficiency disease.