Our data showed the SNO as well as abundance profiles of beta and gamma isoforms of actins (ACTB, ACTG) that are the highly conserved proteins of the cytoskeleton and coexist in most cell types, that are responsible for maintaining the cell integrity, and also are mediators of internal cell motility (Chang and Goldman, 2004) were altered in PBMC of ChD patients (Table 1, Figure 8, Garg et al., 2016). This evidence concerns the gene ACTB and coronary artery disorder.