Since the last 20 years, bacteria of the genus Acinetobacter have been the leading cause of hospital-acquired infections. In addition to the ability of Acinetobacter species to acquire rapid antibiotic resistance, limited knowledge on the mechanisms of multidrug resistance to antibiotics limits the treatment options for such infections. Here, we present a review of cellular processes, including oxidative stress defense, energy metabolism, ppGpp signaling, toxin-antitoxin system, and quorum sensing network in Acinetobacter species and their roles in antimicrobial resistance. Although inhibition of stress responses is an attractive approach to the development of effective antimicrobial therapeutic agents, it is crucial to understand the mechanisms that cause antibiotic resistance in Acinetobacter species, as they are not as well studied as those in other pathogenic bacteria. RelA/SpoT has been shown to be involved in ppGpp synthesis in all 50 genomes of 35 Acinetobacter species. However, toxin-antitoxin (TA) systems are present in less than 30% of the 50 genomes (28/30% of SplT/A; 14/14% of HigB/A; 4/6% of HicA/B), except the RelE/B system (30/78%). These data suggested that ppGpp signaling is conserved in Acinetobacter species, but TA systems are not. This review describes our current knowledge on stress responses with respect to antibiotic resistance or tolerance in pathogenic and non-pathogenic Acinetobacter species.