Acinetobacter baumannii has emerged as a critical nosocomial and environmental pathogen associated with high mortality rates and alarming levels of antibiotic resistance. The World Health Organization has classified A. baumannii as a top-priority pathogen due to its ability to rapidly acquire and disseminate resistance mechanisms. Prevalent in environmental reservoirs such as hospital effluents, agricultural runoff and pharmaceutical effluents, antibiotics’ sub-minimum inhibitory concentrations (sub-MICs) drive resistance evolution in A. baumannii, posing challenges to treatment and public health strategies. This review examines the role of antibiotics’ sub-MICs in driving resistance in A. baumannii across environmental and clinical contexts. Antibiotics’ sub-MICs enhance bacterial resistance by inducing genetic and phenotypic adaptations. These include upregulated efflux pump activities, biofilm formation, horizontal gene transfers, and altered gene expression, enabling A. baumannii to persist in adverse conditions. Environmental reservoirs further exacerbate resistance, with antibiotics’ sub-MICs of tigecycline and colistin promoting adaptive changes in bacterial physiology and virulence. Understanding these pathways in both environmental and clinical settings is essential to develop integrated strategies that mitigate resistance and improve therapeutic options against A. baumannii. This review emphasizes the need to address environmental reservoirs alongside clinical interventions to keep control on the resistance in a one health’s approach.