MDS HSPCs are also known to overexpress toll‐like receptors (TLRs), particularly TLR2 and TLR4, and generate mutated macrophages that have increased NOD‐like receptor protein 3 inflammasome activation and interleukin (IL) 1 beta production, triggering the noncanonical nuclear factor kappa B (NF‐κB) pathway [2, 3, 11]. The gene discussed is NFKB1; the disease is myelodysplastic syndrome.