Proposed model for the impact of DnaK inhibition, using SMR peptide, on biofilm structure and intercellular communication. DnaK, a molecular chaperone, is essential to biofilm formation. Although there is a lack of knowledge on the specific mechanism of DnaK, previous studies have identified DnaK as key to amyloid curli expression within the biofilms of E. coli. We propose that DnaK is required to appropriately fold functional scaffolding proteins that contribute to the structural integrity of a biofilm. Therefore, we propose that therapeutic inhibition of DnaK with the SMRwt peptide resulted in an accumulation of misfolded proteins with subsequent biofilm degradation. In addition, we theorize that the intercellular communication transit of extracellular vesicles was blocked, by SMRwt targeting of DnaK, further exacerbating dysfunction within the biofilm. Created with BioRender.