Antimicrobial resistance (AMR) is a global problem with an extensive health and economic burden driven by various factors, including antibiotic overuse[1]. It is estimated that AMR bacteria will be responsible for as many as 10 million deaths by 2050, exceeding the expected death toll of cancer[2]. Of the numerous bacteria responsible for these deaths, Acinetobacter baumannii is of high concern due to its mortality rate and extensive resistance to widely used treatments such as carbapenems[3-5]. This work applied a peptide-centric/bottoms-up proteomics approach to investigate changes in protein abundance resulting from antibiotic treatment to determine affected biological pathways of an A. baumannii strain treated with either Streptomycin, Cefazolin, or Colistin. Several proteins related to stress responses were noted to be changing in abundance, as well as proteins involved in the maintenance of proteostasis through the conservation of essential housekeeping proteins alongside the decrease or inactivation of the production of several proteins thought of as unessential. Across all treatments, inactivated proteins included those involved in metabolic pathways, increasingly reducing growth in response to antibiotic stress. Specifically in the case of Streptomycin, the lack of detection of the protein product of the annotated resistance gene Aada, detected by previous genomic sequencing, led to the investigation of other proteins changing in abundance, including the uncharacterized proteins F0KG83 and F0KKA7, both of which had been associated with responses to other stresses in other Acinetobacter species. In the case of uncharacterized protein F0KG83, it had been associated with acid or copper resistance, while F0KKA7 has been associated with heat. These differing annotated stress responses across species show an incomplete annotation of these proteins. Further, in the case of Colistin treatment, the lack of a Colistin resistance gene in the tested strain led to the investigation of osmotic shock response through changes in the abundance of porins and mechanosensitive channels as a resistance response to the osmotic shock induced by Colistin. These results revealed several stress responses to antibiotic treatment that were not predicted by genomic sequencing. However, further testing would be required to better understand these mechanisms, either through top-down proteomics in the case of the uncharacterized proteins F0KG83 or testing of different strains and stresses to better understand the role of the inactivation of protein production in the cell's survival.