This was found to occur via a triple crosstalk among CAF, cancer cells, and skeletal muscle: cancer cells stimulate CAF to upregulate secretion of the chemokine CXCL5, which enters the circulation, binds to CXCR2 on skeletal muscle, and activates atrophy-related signaling pathways that drive muscle wasting. Here, CXCL5 is linked to cancer.