Phenotypic diversification in bacteria is driven by natural selection in close correlation with spatial heterogeneity and competition. Since the main source for diversification is mutation, the mechanisms controlling mutation rates may play critical roles in adaptation to new, stressful and heterogeneous environments. Among them, the mismatch repair system (MRS) controls mutation rate by repairing DNA polymerase errors and blocking homeologous recombination events. MRS-deficiency produces a mutator phenotype that has been accounted for as a source of genetic variability. MRS-deficient mutators have been found among natural populations at a frequency much higher than expected, especially in relation to chronic airways infections caused by Pseudomonas aeruginosa in cystic fibrosis (CF) patients. Strong selection of mutators in CF has been related to their higher probability to acquire those mutations needed to continously adapt and persist in the lung. As other persistence strategies, P. aeruginosa colonizes the respiratory track growing as biofilm communities and diversifying into specifically adapted phenotypes. Mainly defined by oxygen and nutrient limitations, biofilms are constituted by micro-niches shaping a heterogeneous environment where adapted phenotypes need to be selected for. Could mutators, diversification and biofilm mode of growth interplay in P. aeuroginosa adaptation? Flow-cell biofilms was the system through wich P. aeruginosa mutator biofilms were exhaustively characterized. Our findings support how MRS-mutator cells may speed adaptation to the biofilm mode of growth by fastening genetic useful variation.