IL10 and neoplasm: Suboptimal CAR T cell persistence and function in the tumor microenvironment (TME) further derives from exposure to inhibitory soluble mediators such as TGFβ, IL10, and adenosine; interaction with suppressive immune populations such as regulatory T cells, myeloid-derived suppressor cells (MDSCs), and tumor-associated macrophages; and engagement of inhibitory ligands that promote exhaustion and or apoptosis of T cells3.