Unlike the PD‐1/PD‐L1 axis, which activates restricted subsets of T cells in the tumor microenvironment and in circulation, CTLA‐4 inhibition induces the breadth of T cell activation,174, 175 which is thought to be responsible for the high rate of immune‐based toxic effects during treatment or even long after treatment cessation. Here, CD274 is linked to neoplasm.