Most inflammatory processes seem to require the release of the S100A8/A9 heterodimer into the ECM.153–155 Significant upregulation of S100A8/A9 has been observed in many tumors, including lung, gastric, esophageal, colon, pancreatic, bladder, ovarian, thyroid, breast, and skin cancers.156,157 The upregulation of S100A8/A9 is caused either by the infiltrating immune cells of tumor microenvironment158 or by the tumor itself,156,157 contributing to the establishment of a pre-metastatic niche in the tumor microenvironment.159. This evidence concerns the gene S100A8 and skin neoplasm.