S100A8/A9 stimulates the production of ROS in a STAT3-dependent manner, leading to nitration of the TCRαβ, thus rendering the T cells incapable of interacting with the antigen bound in the major histocompatibility complex II (MHC-II) of the antigen-presenting cells (APCs) and initiating the anti-cancer response [24]. This evidence concerns the gene S100A8 and cancer.