Although the exact role for TLRs in CM remains to be elucidated, a number of studies suggest that the pathogenesis of PbA-induced SM is independent of TLR4[20], unlike the pathogenesis of sepsis where mice deficient in TLR4 are highly resistant to the development of LPS-induced septic shock[21]. The gene discussed is TLR4; the disease is systemic mastocytosis.