Ultimately, the IFNγ-dependent bystander killing effect for solid tumors relies upon the tumor microenvironments in solid tumors, as their environments can have confined spaces of stromal, cancer and extracellular matrix components that can enable greater concentrations of cytokines like IFNγ, allowing for increased ICAM-1 (intercellular adhesion molecule) expression on neighboring tumor cells and increased CART cell engagement [9,10]. The gene discussed is ICAM1; the disease is neoplasm.