Intriguingly and in line with our proposed model of GLI-dependent IDO1 expression, treatment of IFNγ-stimulated melanoma cells with the GLI inhibitor HPI-1 reinstated the proliferation of CD4+ and CD8+ T cells like epacadostat (Fig. 5C, D), providing functional evidence for a role of HH/GLI signaling as immunosuppressive driver via enhancing IDO1 expression and kynurenine production in the tumor microenvironment (Fig. 5E). The gene discussed is CD4; the disease is melanoma.