discovered that TET2 expression was enhanced in an IL1R/MyD88 pathway-dependent manner in TAMs isolated from both murine and human melanoma specimens, and myeloid-specific ablation of Tet2 led to suppressed melanoma growth in vivo by modulating the gene expression program from an immunosuppressive status into a proinflammatory status in TAMs (64). This evidence concerns the gene IL1R1 and melanoma.