Objectives. The objective of this study was to improve the knowledge regarding the mechanisms of antimicrobial resistance of Staphylococcus aureus strains in order to prescribe effective and quality antimicrobial treatments. Material and methods. The analysis of publications in PubMed was carried out between January and November 2022 regarding the theoretical aspects of the antimicrobial resistance mechanisms characteristic of Staphylococcus aureus strains, by using the key terms "Resistance mechanisms", "Resistance genes", "Staphylococcus aureus" and " Antimicrobial preparations". From the total number of articles found (44), 27 synthesis and meta-analysis articles reflecting the mechanisms of antimicrobial resistance of Staphylococcus aureus strains were selected and analysed. Results. The initial resistance of S. aureus to β-lactams arose through the production of βlactamases. The target of β-lactam antibiotics is the transpeptidase fragment of penicillinbinding protein (PBP)-2. PBP2a is not sensitive to β-lactams because the target serine of the active site of PBP2a is located in a deep sleeve that cannot be reached by antimicrobials. This structural change is very significant because it makes the serine at the active site inaccessible to all β-lactams, thus making MRSA resistant to this class of antimicrobials. Vancomycin resistance in S. aureus can come in two forms: vancomycin-resistant S. aureus (VRSA) and vancomycin-intermediately resistant S. aureus (VISA). Except for a few cases, resistance to vancomycin has occurred in methicillin-resistant strains of S. aureus. It should be noted that the mechanisms of VISA and VRSA are completely different, and therefore VISA strains cannot gradually progress to become VRSA. However, in extremely rare cases, when VISA strains acquire additional resistance mechanisms, such as the vanA operon, they can become VRSA, but by a totally different mechanism. Conclusions. The unargued and unjustified use of antimicrobial preparations has led to the development of resistance to them in S. aureus strains. This species may better than any other human pathogen exemplifies adaptive evolution to antimicrobials, as it has demonstrated a unique ability to rapidly respond to each new antibiotic by developing a resistance mechanism, beginning with penicillin and methicillin, up to the newer, linezolid and daptomycin. Mechanisms of resistance include enzymatic inactivation of the antibiotic, modification of the target of attack, uptake of the antibiotic, and efflux pumps. By knowing the basics of antimicrobial resistance mechanisms, the clinician can indicate appropriate antimicrobial treatment for the pathogen in question.