Ribosomes, the universal cellular nan-machines that translate the genetic code into proteins, are targeted by many antibiotics that paralyze them by binding to their functional sites. The three-dimensional structures of complexes of ribosomes from genuine pathogens and pathogen-model with ribosomal antibiotics revealed their binding modes, inhibitory actions and synergism pathways. They also indicated the principles of differentiation between patients and pathogens, suggested the species-specific mechanisms leading to bacterial resistance, and paved the way towards improvement of existing antibiotics, as well as towards the design of advanced therapeutics capable of minimizing antibiotic resistance.