As a result, increased ROS production also led to higher IFN-γ, IL-6, and TNF-α cytokine expression and consequently increased expression of CD8+ T cells and CD4+/Treg ratio as well as concurrent reversion of the immunosuppressive TME, thereby effectively inhibiting tumor development by turning a “cold” tumor into a “hot” one [138]. The gene discussed is CD8A; the disease is neoplasm.