In "C. albicans", resistance occurs by way of mutations in the "ERG11" gene, which codes for 14α-demethylase. These mutations prevent the azole drug from binding, while still allowing binding of the enzyme's natural substrate, lanosterol. Development of resistance to one azole in this way will confer resistance to all drugs in the class. Another resistance mechanism employed by both "C. albicans" and "C. glabrata" is increasing the rate of efflux of the azole drug from the cell, by both ATP-binding cassette and major facilitator superfamily transporters. Other gene mutations are also known to contribute to development of resistance. "C. glabrata" develops resistance by up regulating CDR genes, and resistance in "C. krusei" is mediated by reduced sensitivity of the target enzyme to inhibition by the agent.