Despite many years of investigation, it is not clear how gentamicin and other aminoglycosides cause bacterial cell death. It is known that gentamicin binds irreversibly to one of two aminoglycoside-binding sites on the 30 S ribosomal subunit, which, in turn, inhibits bacterial protein synthesis. However, inhibition of bacterial protein synthesis does not adequately explain gentamicin's bactericidal effects, since other non-aminoglycoside antibiotics that also inhibit protein synthesis are only bacteriostatic. One aspect essential to aminoglycoside lethality is the need to achieve intracellular concentrations in excess of extracellular. Anaerobic bacteria are not susceptible to aminoglycosides due, at least in part, to a lack of an active transport mechanism for aminoglycoside uptake.