Despite extensive research, standard treatment for Marfan syndrome (MFS) is mainly limited to slowing down thoracic aortic aneurysm (TAA) progression by administering beta-blockers and/or angiotensin receptor blockers (ARBs). When indicated prophylactic aortic root surgery can be performed to lower the chance of dissection and potentially lethal rupture of the aorta. This surgery has the greatest impact on reducing mortality in MFS patients. However, it still holds many risks, comes at a higher cost, and cannot fully exclude that dissection or rupture will not occur. So, if surgery could be avoided by improving standard treatments, it would enhance patients’ health outcomes and reduce societal costs. TGF-beta is already known as one of the key-players in the development of TAA in MFS patients, but an increase in TGF-beta levels is also observed in many other diseases such as fibrosis, autoimmune diseases, and cancers. However, the exact contribution of this increase in TGF-beta to the pathogenesis of these diseases remains unclear. With the TGF-beta reporter we generated, it is possible to monitor TGF-beta levels over time and in different zebrafish models. In the future these results together with other research could potentially unravel the role of TGF-beta in the pathogenesis of TAA-related diseases but could also lead to a breakthrough in understanding the pathogenesis of other diseases such as certain cancer syndromes. These insights can drive the development of new therapies and thereby improve health outcomes in patients and lower societal costs.