Notably, the absence of NLRP3 exclusively in CD4+ T cells is sufficient to replicate the slowed tumor growth observed in mice completely deficient in Nlrp3. These findings indicate that the deleterious role of NLRP3 in other cell types (such as myeloid cells), particularly through IL-1β secretion, may be compensated for by the blockade of NLRP3 in CD4+ T cells. This evidence concerns the gene IL1B and neoplasm.