Linear-effect model is the most common hypothesis on how CNVs function in disease, and the findings in the CNV-loci 16q22.1 (Armitage trend test P value = 3.98×10−8, the trend also shows in clustering heat map) can support this hypothesis: amplification of two genes (PDPR and AARS) in 16q22.1 might impose a counteractive effect on CAD, while loss of copy number may cause weaker recovery from heart attack as they function in post-ischemic heart [32], [33]. The gene discussed is PDPR; the disease is coronary artery disorder.