The interest in PCSK6 as a therapeutic target in CVD could be attributed to its processing of various proteins involved in different stages of atherosclerosis development, such as suppressing the activity endothelial and lipoprotein lipase, preventing the release of free fatty acids from HDL particles (Choi and Korstanje, 2013), processing GDF-15 that increases inflammatory response (Wang et al., 2019) as well as PDGFB and MMP14 responsible for SMC migration (Rykaczewska et al., 2020). This evidence concerns the gene LPL and atherosclerosis.