Statins, drugs from the group od bypolipemics, are one of the most prescribed drugs worldwide because of their safety, big efficiency and few side effects. Statins reduce plasma cholesterol and LDL lipoproteins in the blood. The primary mechanism of action is inhibition of HMG CoA reductase, the limiting enzyme in the biosynthesis of cholesterol. Numerous secondary mechanisms: reducing oxidative stress, stabilizing atherosclerotic plaques, neuroprotective and immunomodulatory mechanism still remain unexplored. Population studies that have included people with cardiovascular disease, hyperlipidemia, and a history of statin therapy indicated potential connection between altered glycosylation of plasma proteins and statin therapy. Glycosylation, among the other roles, has an important immunomodulatory role in directing IgG response from proinflammatory to anti-inflammatory and vice versa. Possible connection between immunomodulatory effect of statins and glycan changes in plasma proteins or lgG was examined in this paper analysis of glycosylation of plasmna proteins and immunoglobulin G before and after taking statin therapy (rosuvastatin). To confirm the reliability of the results, the trial included a control group which took placebo during the same period of time. Analysis of N-glycans of plasma proteins were performed by HILIC UPLC, while the analysis of IgG subclasses glycosylation included nano LC-ESI-MS. Statistical analysis of the obtained results using the R programe compared glycosylation profiles of statin therapy group and control placebo group. Mann Whitney U test did not show any statistically significant difference between the two groups, what leads to conclusion that statin therapy with rosuvastatin does not alter the glycosylation profile of N-glycans of plasma proteins, nor glycosylation of immunoglobulin G subclasses. This study demonstrated that there was no effect of statins (rosuvastatin) on glycosylation.