The toxin has an active A domain, a binding B domain, and a hydrophobic segment, the T domain. The A domain catalyzes the transfer of an adenosine diphosphate-ribose molecule to one of the elongation factors responsible for protein synthesis. This transfer can inactivate the factor and inhibit protein synthesis, which can cause cell death. Cell death by toxin is the keynote of the pathogenesis, and the prevention of diphtheria by vaccination with toxoid is the keynote of successful epidemiologic control.