Immunotherapy, a treatment that increases the survival of cancer patients to the point of remission of the disease, can also have the opposite effect. In some patients, immune checkpoint blockade accelerates cancer. Now, researchers at the University of Michigan Medical School have discovered that the answer to this hyperprogressive disease (HPD) lies in the interconnection of the molecular pathways of interferon signaling (IFNγ), fibroblast growth factor 2 (FGF2) and the β-catenin protein.