Immune and non-immune cells (stroma) within the tumor microenvironment (TME), along with factors produced by those cells, play important roles in tumorigenesis. In early stages of tumor growth tumor-antagonizing immune cells/factors within TME seem to inhibit growth of cancer cells, while at later stages, escape from, or even inhibition of the effector function(s) of tumor-antagonizing immune cells, can occur. Tumor-associated stromal cells (TASCs), novel stromal cells in the inflammatory TME which develop after long-term interaction with tumor cells, express higher levels of multiple proteins compared with their normal non-reactive counterpart. In addition they secrete pro-tumorigenic factors, including IL-6, IL-8, Vascular Endothelial Growth Factor (VEGF), and matrix metalloproteinases, all of which contribute to augmented recruitment of tumor and pro-tumorigenic cells to the microenvironment. The immune evasion capability of tumors (tumor checkpoints) has been studied leading to the development of clinical strategies which target molecules associated with checkpoint inhibition. Use of immune checkpoint inhibitors, as exemplified by the use of anti- CTLA4 and anti-PD antibodies, along with adoptive transfer of engineered immune cells.