Muscle atrophy is the most common complication in cancer cachexia patients, resultsing in a serious prognosis. Various drugs for muscle atrophy have effects on the remission of cancer cachexia. Among them, the regulatory role of JAK/ STAT3 has attracted attention. In recent years, the mechanism of JAK/ STAT3 signaling regulating sarcopenia in cancer cachexia and related drug intervention has been studied in basic research and clinical experiments. These studies concluded that the JAK/ STAT3 signaling pathway can regulate muscle atrophy in cancer cachexia through the ubiquitin proteasome system, the autophagy lysosome system, microRNA and the tumor microenvironment. Specific drugs can effectively alleviate the process of cancer cachexia muscle atrophy by interfering with the JAK/ STAT3 signaling pathway.