In initial studies centered in mice it was shown that RAG1-deficient/IL-10Rβ-deficient mice adoptively transferred IL1-deficient CD4+ T cells manifested less colitis and less pro-inflammatory cytokine production than the same mice transferred WT CD4+ T cells presumably because in the former instance the transferred IL-1r-deficient T cells were not responsive to the excessive IL-1β produced in mice whose NLRP3 inflammasomes was not inhibited by IL-10. The gene discussed is IL1B; the disease is colitis.