The heightened immune activity in “hot” tumors makes them prime candidates for effective immunotherapy responses, including checkpoint inhibitors (such as anti-PDL1 and anti-CTLA4), which restore T cell function by blocking inhibitory pathways, and CAR (Chimeric Antigen Receptor) T cell therapy, which harnesses genetically engineered T cells to target and kill cancer cells [12,13]. Here, CTLA4 is linked to cancer.