Specifically, it caused significantly decreased expression of Treg cell markers such as Foxp3, CD25 and Helios and genes required for optimal Treg cell function and immunosuppression in the TME, such as Tgfb1 or Gzmb. Thus, c-Rel inhibition reduced Treg cell activity in the TME resulting in reinforcement of anti-tumor immunity, attenuation of tumor growth and potentiation of anti-PD-1 therapy without causing autoimmunity (96). The gene discussed is PDCD1; the disease is neoplasm.