Multidrug resistance is one of the principle challenges in health sciences today. æSome microbial species develop resistances quickly and others do not. æWhy this is so is unknown, thus is a critical gap in our knowledge because it directly relates to how we will combat the multidrug resistance. The principle objective of this study is to check the following specific hypothesis: whether or not the ability to acquire antibiotic resistances stems from the ability to mutate. æWe hypothesize that there is a correlation between the presence of multiple error prone DNA polymerase genes to higher mutatagenic potential and better survivability in the presence of drugs. æAn important multiple drug resistant pathogen Acinetobacter baumannii, contrasted to a non-resistant Escherichia coli, will serve as our model system.