IL‐33 receptors ST2 and, above all, MyD88, which was required for the IL‐33‐mediated increase in the number of myeloid DCs, cooperate to induce the expression of co‐stimulatory molecules on myeloid DCs in response to recombinant IL‐33, thus revealing a novel IL‐33‐ST2‐MyD88‐STAT1 axis that restores the activation and maturation of myeloid DCs in cancer.92 This evidence concerns the gene MYD88 and cancer.