PLYΔ146/147 was not able to bind to the membranes at all and had no detectable hemolytic activity (Figure 7B). Ionic interactions between the β-strands thus contribute significantly to pore stability, and any disruption of these interactions compromises pore formation. Both mutations pinpoint protein regions that are promising targets for drug development. Drugs that interfere with these interactions would render the toxin ineffective, and the bacteria that produce it non-pathogenic.