Cystic fibrosis (CF) is one of the most common recessively inherited rare diseases, affecting over 70000 people worldwide. The most common cause of mortality in CF is chronic lung infection with Pseudomonas aeruginosa - a virulent pathogen that is highly antibiotic resistant and is virtually impossible to eradicate once established. Successful treatment of P. aeruginosa infections is hampered by rapid evolutionary adaptation of P. aeruginosa within the lung, leading to a diverse resident P. aeruginosa population of highly virulent and multidrug-resistant subtypes. However, we do not yet understand the drivers of P. aeruginosa evolution over the course of a chronic infection, making it difficult to predict how the pathogen will respond to treatment. However, experimental evolution can help pinpoint key drivers of diversity in clinically-relevant P. aeruginosa phenotypes. I will discuss our work revealing the extensive P. aeruginosa phenotypic diversity in the CF lung, as well as how we have employed experimental evolution to understand how biotic and abiotic factors shape P. aeruginosa evolutionary trajectories.