Modelling the asthma risk (Glu) residue in place of Ala78 appears to alter the local structure and so may influence the electrostatics of the region pertaining to the Arg64‐Asp81 and Glu28‐Lys109 salt bridges and therefore indirectly modify ligand binding through overall disruption of the shape/conformation of the IL33 binding site. The gene discussed is IL33; the disease is asthma.