To explore a direct role for LKB1-deficient DCs in promoting Th17 responses, we sorted hepatic cDC2s, the main CD4+ T cell–priming subset shown to induce Th17 priming (28), from lean CD11cWT and CD11cΔLKB1 mice that were s.c. injected with Flt3L-secreting B16 melanomas to expand the in vivo DC pool (Figure 5A). This evidence concerns the gene FLT3LG and melanoma.