The increasing incidence of pathogenic fungi resistant to treatment with amphotericin B (AmB) has created a demand for novel anti-fungal agents that can circumvent the pathogens¿ resistance, and the successful development of such compounds will clearly require an understanding of the drug¿s mechanism of action at the molecular level. It has long been held that AmB exerts its anti-fungal action through the generation of self-assembled ion channels formed in the ergosterol-containing fungal cell membranes, but not in the cholesterol-containing human cell membranes. There is no direct structural evidence to support this hypothesis, however, and recent research suggests it is seriously flawed. In the SANS studies proposed here, we seek to understand how differences in a sterol¿s chemistry influence its effects on biomembrane structure, and how these then affect AmB membrane interactions.