Antibiotic resistance is one of the major threats to human society prompting an urgent global response. Bacteria developed multiple strategies for antibiotic resistance by effectively reducing intracellular antibiotic concentrations or antibiotic binding affinities to their specific targets. In this talk, I will present a recently discovered pathway to antibiotic resistance that depends on the bacterial morphological transformation that promotes bacterial decrease of antibiotic influx to the cell. By analysing cell morphological data of different bacterial species under antibiotic stress, we find that bacterial cells robustly reduce the surface-to-volume ratio in response to most types of antibiotics. Using quantitative modelling we show that by reducing the surface-to-volume ratio, bacteria can effectively reduce intracellular antibiotic concentration by decreasing antibiotic influx. The model predicts that bacteria can also increase the surface-to-volume ratio to promote antibiotic dilution for membrane-targeting antibiotics, in agreement with data on membrane-transport inhibitors. Using the particular example of ribosome-targeting antibiotics, I will present a systems-level model for the regulation of cell shape under antibiotic stress and discuss feedback mechanisms that bacteria can harness to increase their fitness in the presence of antibiotics.