Molecular chaperones have central role in the maintenance of a functional proteome in the cell. The mitochondrial chaperone Trap1 is a member of the Hsp90 family. Aim of this thesis project is to describe functional aspects of Trap1. We knew that cells lacking Trap1 acquire bigger size. Here we identified that these cells also acquire higher DNA content and we excluded known regulators of cells size, such as mTOR pathway, as the reason of the increased cell size. Interestingly, we were able to observe that ROS is a potential candidate of cell size regulation. Additionally, we described that mice devoid of Trap1 have impaired glucose homeostasis. Moreover, by using a mouse genetic breast cancer model we noticed a delay in tumor onset in the absence of Trap1. Overall, this work proposes new functional aspects of Trap1. Further investigation in order to identify the molecular mechanisms involved is needed.