Have you ever imagined that research on a three-centimeter animal could probably have a global impact. Up until today Marfan syndrome (MFS) is a condition that affects a lot of people’s lives worldwide and for which a curative treatment has still not been found. This syndrome is a connective tissue disorder which is caused by variants in the DNA, more specific in the gene called FBN1. These variants result in a defective connective tissue protein called ‘fibrillin’. Many different organ systems are affected including the cardiovascular system. Cardiovascular complications such as dilation of the aortic root (which is the beginning of the aorta) and aortic dissection (the formation of a second lumen) must be avoided due to the high mortality rate. A lot of research has been done in mouse models, but the zebrafish also seems to be a suitable animal model due to many new possibilities e.g. easy genetic manipulation. Animal models permit researchers to gain a better understanding of the disease mechanisms and to look for a curative treatment based on these mechanisms. The Zebrafish appears to be a promising model because this animal is very similar to humans. In addition, research is very progressive because of the larger number of offspring that can be obtained. Another major advantage is the fact that analysis can be done at embryonic and adult stages. For now, this domain is more ‘unknown territory’ that needs further mapping. Once a suitable zebrafish model is found, research about disease development and treatment will gain momentum. This master thesis will zoom in on the possible abnormal cardiovascular structures found in genetically modified zebrafish, specifically with a variant in the 'fbn2b gene'. This will be compared with zebrafish without this genetic variant. Thus, the main focus of the thesis will be on the bulbus arteriosus, atrium, ventricle, atrioventricular valves and ventriculobular valves. The social impact of this master thesis is not negligible, since MFS is one of the most common rare connective tissue diseases and has a worldwide incidence. Once it is demonstrated that a suitable zebrafish model exists for MFS, it will be possible to investigate the still unknown mechanisms of this disorder. It will also be possible to investigate new treatments that can be implemented in future practice and which could lead to a decrease in morbidity and mortality.