Acinetobacter baumannii is a Gram-negative opportunistic nosocomial pathogen. This microorganism survives in hospital environments despite unfavorable conditions such as desiccation, nutrient starvation and antimicrobial treatments. It is hypothesized that its ability to persist in these environments, as well as its virulence, is a result of its capacity to form biofilms. A. baumannii forms biofilms on abiotic surfaces such as polystyrene and glass as well as biotic surfaces such as epithelial cells and fungal filaments. Pili assembly and production of the Bap surface-adhesion protein play a role in biofilm initiation and maturation after initial attachment to abiotic surfaces. Furthermore, the adhesion and biofilm phenotypes of some clinical isolates seem to be related to the presence of broad-spectrum antibiotic resistance. The regulation of the formation and development of these biofilms is as diverse as the surfaces on which this bacterium persists and as the cellular components that participate in this programmed multistep process. The regulatory processes associated with biofilm formation include sensing of bacterial cell density, the presence of different nutrients and the concentration of free cations available to bacterial cells. Some of these extracellular signals may be sensed by two-component regulatory systems such as BfmRS. This transcriptional regulatory system activates the expression of the usher-chaperone assembly system responsible for the production of pili, needed for cell attachment and biofilm formation on polystyrene surfaces. However, such a system is not required for biofilm formation on abiotic surfaces when cells are cultured in chemically defined media. Interestingly, the BfmRS system also controls cell morphology under particular culture conditions.