While additional studies on the interplay between NLRP3, ER stress, and consequently eIF2 phosphorylation are necessary, our results indicate that targeting NLRP3 in AML patients may provoke ER stress, phosphorylation of eIF2α, and consequently apoptosis of AML blasts, thus providing a potential novel therapeutic strategy. The gene discussed is EIF2A; the disease is acute myeloid leukemia.