The efflux pumps, beside the class D carbapenem-hydrolysing enzymes (CHLDs), are being increasingly investigated as a mechanism of carbapenem resistance inAcinetobacter baumannii. This study investigates the contribution of efflux mechanism to carbapenem resistance in 61 acquiredblaCHDL-genes-carryingA. baumanniiclinical strains isolated in Warsaw, Poland. Studies were conducted using phenotypic (susceptibility testing to carbapenems ± efflux pump inhibitors (EPIs)) and molecular (determining expression levels of efflux operon with regulatory-gene and whole genome sequencing (WGS)) methods. EPIs reduced carbapenem resistance of 14/61 isolates. Upregulation (5–67-fold) ofadeBwas observed together with mutations in the sequences of AdeRS local and of BaeS global regulators in all 15 selected isolates. Long-read WGS of isolate no. AB96 revealed the presence of AbaR25 resistance island and its two disrupted elements: the first contained a duplicate ISAba1-blaOXA-23, and the second was located betweenadeRandadeAin the efflux operon. This insert was flanked by two copies of ISAba1, and one of them provides a strong promoter foradeABC, elevating theadeBexpression levels. Our study for the first time reports the involvement of the insertion of the ΔAbaR25-type resistance island fragment with ISAba1element upstream the efflux operon in the carbapenem resistance ofA. baumannii.