It was also reported that an increase in C26-tumor-derived serum levels of S100B and high mobility group box 1 (HMGB1) leads to persistent activation and overexpression of the receptor for advanced glycation end-products (RAGE), a protein-inducing key-changes characteristic for CC (e.g., muscle wasting, systemic inflammation, and release of tumor-derived procachectic factors) [147]. This evidence concerns the gene S100B and neoplasm.