The gene encodes the sterol C24-methyltransferase converting zymosterol to fecosterol in the ergosterol biosynthetic pathway. Here, we extend the results of functional analysis of the gene, which was previously shown to modulate drug susceptibility in mutant cells, by demonstrating that its deletion leads to increased susceptibility to cycloheximide, 4-nitroquinoline-N-oxide and weak organic acids, and such effects are associated with attenuated virulence. Together with abrogated efflux of drug substrates by Cdr1p and Pdr12p, the mutation leads to reduced cell surface hydrophobicity and decreased virulence of the mutant cells of . The absence of Erg6p impacts the lipid organization and function of the plasma membrane, resulting in non-specific permeability and abrogation of normal function of membrane-bound proteins accompanied by decreased virulence in cells. larvae were used as a non-vertebrate animal host model to determine differences in the virulence potential of strains (parental strain and the deletion mutant). We found that mutant strain attenuated in virulence caused 25-30% survival of larvae compared with parental strain.