Mice with TKTB6-RAS–derived tumors, which grew relatively slower than TKTB34-RAS–derived tumor, owing to lower HRASG12V expression levels, demonstrated elevated CXCL1 levels suggesting a correlation between circulating CXCL1 and mutant RAS-induced skeletal muscle defect. The gene discussed is CXCL1; the disease is neoplasm.