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. The gene discussed is PDCD1; the disease is neoplasm.