Recent stoichiometric analysis of the D299G and T399I polymorphic variants of TLR4 confirmed that the presence of each of the D299G and T399I variants results in distinct structural changes in the ligand-binding site of the receptor [32], which account for increased susceptibility to infectious disease such as Gram-negative sepsis [9] and malaria [31], [33]. The gene discussed is TLR4; the disease is infectious disease.