The mechanism driving CDK12‐altered tumor sensitivity to immune checkpoint inhibitors lies in the association between CDK12‐loss‐of‐function mutations with a higher focal tandem duplication burden; focal tandem duplications lead to increased production of fusion‐induced neoantigens that can be responsive to PD‐1/PD‐L1 blockade.10 The gene discussed is CD274; the disease is neoplasm.