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Carbapenem resistance is mainly mediated by carbapenemases or extended-spectrum β-lactamases (ESBL) plus a loss of porins. However, we have identified a clinical isolate that contains neither carbapenemases nor ESBLs. Instead, we found that high-level expression of a novel -derived β-lactamase gene, , in conjunction with OmpK36 deficiency results in high-level carbapenem resistance. This finding demonstrates the combinatorial complexity of factors, including β-lactamase activity, its expression levels, and porin activity, that yield carbapenem resistance.