The presence of concurrent CAD did not result in any statistical difference in either median HSP27 (1.88 ng/mL versus 1.86 ng/mL in those with and without CAD respectively) or the proportion below the optimal binary threshold of 2.69 ng/mL (69.6% versus 70.3%, with and without respectively, p = 0.87). This evidence concerns the gene HSPB1 and coronary artery disorder.