Besides effects on gene expression, another possible mechanism that could account for the effects of the rs6318 C allele on the function of the 5HTR2C receptor that increase cortisol responses to stress (and thereby affect clinical outcomes in CHD patients) is that substitution of serine for a cysteine residue in 5HTR2C protein among C allele carriers could result in disruption of disulfide bridges that play a critical role in the folding of a protein into its native conformation [36]. This evidence concerns the gene HTR2C and coronary artery disorder.