Pseudomonas aeruginosa is an opportunistic human pathogen, and displays a particular predilection for infecting soft tissues such as those in the respiratory tract. Indeed, in individuals who are genetically predisposed towards P. aeruginosa infection (such as people with cystic fibrosis (CF)) the organism poses an existential threat, and such infections require intensive long‐term management. Unlike Escherichia coli, which displays a strong preference for metabolizing sugars, P. aeruginosa is metabolically "wired up" to consume fatty acids, which are abundant in the CF airways. However, the details of how P. aeruginosa carries out the feat of beta oxidation (required to metabolize fatty acids) have only recently become clear. This is particularly true of the acyl‐CoA dehydrogenase enzymes, and in this presentation, I will show how the enzymology at this bottleneck has been elucidated and why this is important. I will also discuss the fate of the acetyl‐CoA produced during beta oxidation, since this is a nice example of the dangers inherent in extrapolating biological insight from one well‐characterized model organism (E. coli) onto others, such as P. aeruginosa. Finally, it is worth noting that P. aeruginosa rarely lives in "splendid isolation" (to paraphrase Foster), but instead, shares the CF airway ecosystem with a veritable "zoo" of other microbes. Gaining experimental traction with such polymicrobial systems has been challenging, but recent work indicates that these co‐habitants can exert a profound influence on one another's biology.