CCS members of the University of Salzburg and the Salzburg Cancer Research Institute unravel the molecular and cellular mechanisms of how activation of hedgehog (HH) signaling induces non-melanoma skin cancer and establishes an immunosuppressive tumor microenvironment. HH signaling inhibits the activity of antitumoral T cells via programmed death ligand 1/programmed death‐1 immune checkpoint signaling and the recruitment of immunosuppressive regulatory T cells. Skin cancers/basal cell carcinoma also show strong infiltration with antitumoral neutrophils. The data support the evaluation of combination treatments with HH inhibitors and immune checkpoint blockers. The study, which was done in collaboration with the Medical Universities of Innsbruck and Vienna, has been published in the latest issue of Molecular Oncology (Grund-Gröschke et al., Mol. Oncol 2020).