This article reviews current knowledge of the mechanisms of resistance of Acinetobacter spp to antimicrobial agents. As will be seen although the evidence has not been completely demonstrated, it seems that a decrease in membrane permeability, in conjunction with a probable active efflux system, confers an important intrinsic resistance on this microorganism. This natural resistance may be increased by resistance acquired by the transfer of genetic elements (plasmids, transposons and integrons), as in the case of β-lactamase acquisition (TEM-1, TEM-2, OXA-21) or the aminoglycoside-modifying enzymes (APH(3')VI, AAC(3)Ia). This transfer may take place by conjugation or natural transformation, and both processes occur not only in animate (e.g. the skin, the gastrointestinal tract) but also in inanimate reservoirs. Moreover, the selective pressure exercised by the antibiotic in these reservoirs may select resistant mutants (e.g. resistance to quinolones). Thus, Acinetobacter, and more specifically A. baumannii, has all the necessary conditions to acquire multiresistance and it may therefore be considered the paradigm of multiresistant bacteria.