This attenuation of infiltrating T cell responses was driven by Jag1/2 expressed by immunosuppressive myeloid-derived suppressor cells (MDSCs) which could be overcome by ectopic expression of Notch1 intracellular domain (N1ICD) in antigen specific T cells, indicating that the TME is programmed with mechanisms to suppress Notch signaling and evade T cell-mediated tumor cell death. Here, JAG1 is linked to neoplasm.