Vascular malformations are the result of atypical development of blood vessels. As with many rare conditions, vascular malformations are understudied, and the mechanisms underlying their formation remain poorly understood. In this work, I use the tracheal system of Drosophila as a model for studying vascular development. Drosophila, with its genetic similarities to humans and ease of study, serves as an ideal model organism. More specifically, the Drosophila tracheal system highly resembles the human vasculature, providing valuable insights into human vascular development. Ciboulot, identified through RNA sequencing, encodes a protein vital for maintaining cell structure. To understand its role in tracheal development, RNA interference was used to reduce the level of Ciboulot proteins expressed in tracheal cells, leading to observed deficiencies in terminal cell formation within the trachea. Specifically, larvae with reduced Ciboulot expression exhibited a significant increase in missing terminal cells compared to the control larvae. Terminal cells are highly branched cells that supply oxygen to nearby tissues. These findings emphasize the critical involvement of Ciboulot in terminal cell formation, highlighting its necessity for proper tracheal development. Future experiments will further investigate this requirement by exploring when this abnormality arises in Drosophila through the use of live imaging of Drosophila embryos. Overall, my research underscores the importance of Ciboulot in Drosophila tracheal system development, paving the way for further investigations into its role in human vascular development and associated disorders.