Zhao et al. [40] demonstrated that melanomas generate a site of immune privilege by driving DCs fatty acid oxidation via a Wnt5a-b-catenin-PPAR-γ signaling pathway that culminates in the induction of IDO enzyme activity, and this study also showed that inhibiting this pathway reverses DCs tolerization and enhances anti-PD-1 antibody efficacy in a transgenic model of melanoma. The gene discussed is IDO1; the disease is melanoma.