IL-18–IL-18R–MyD88 signaling has been shown to trigger the recruitment of TIR domain-containing IRAK4, leading to the activation of JNK that promote CD8+ T cell-mediated tumor immune surveillance.41–44 Moreover, SIGIRR inhibited IL-18-induced activation of IRAK4 and JNK protein kinases signaling in NK cells.38 In present study, we explored molecular signaling downstream exerted by IL-37, IRAK4, and JNK phosphorylation in cytotoxic T cells was assessed by flow cytometry and western blotting. Here, SIGIRR is linked to neoplasm.