This dual behavior is consistent with findings by Melvin et al., who reported that while elevated levels of both galectin-3 and pentraxin-3 in patients with stable CAD were associated with increased cardiovascular risk, the biomarkers act through non-redundant pathways—galectin-3 reflecting fibrotic stress and pentraxin-3 suggesting an adaptive or compensatory immune mechanism. This evidence concerns the gene PTX3 and coronary artery disorder.