The question gives three overlapping descriptors - diphtheria toxin, AB exotoxin, ADP-ribosylation - which are really three facets of the same answer. The molecular event being asked about is inactivation of elongation factor 2.
Diphtheria toxin is a two-component (A-B) exotoxin. The B fragment binds and delivers the A fragment into the cytosol, where the A fragment transfers an ADP-ribose group from NAD$^+$ onto diphthamide, a modified histidine residue found only on EF-2:
$\text{EF-2} + \text{NAD}^+ \xrightarrow{\text{toxin A}} \text{EF-2-ADP-ribose} + \text{nicotinamide}$
Once ADP-ribosylated, EF-2 can no longer drive ribosomal translocation, so translation stops and the cell dies. Cholera and E. coli LT toxins also ADP-ribosylate, but their target is Gsalpha, not EF-2, producing secretory diarrhoea rather than cytotoxicity. Hence the EF-2 inhibitor is the diphtheria toxin.
\[\boxed{\text{Diphtheria toxin (ADP-ribosylates EF-2)}}\]