Of note, only S100A9 was uniquely elevated in the “unfit” group; the role of this protein in mediating inflammation has been elegantly reviewed previously [85], with emerging evidence now linking elevated S100A9 to skeletal muscle mitochondrial fragmentation [86], pancreatic cancer–associated cachexia [87], sarcopenia in kidney disease patients [88], and insulin‐independent anti‐diabetic effects in Type 1 diabetes [89]. This evidence concerns the gene S100A9 and pancreatic neoplasm.