Candida albicans is a dimorphic fungus, have the ability to secrete a quorum sensing molecule farnesol in a cell density dependent manner which regulates its morphogenic shift from yeast to hyphae. The ability to switch between different forms is highly correlated with its ability to cause disease such as Candidiasis. The switching between different yeast to hyphae form leads to significant alteration in the plasma membrane sphingolipids. Complex sphingolipids are principal components of fungal plasma membranes; and their interaction with antifungal drug can play a crucial role in multidrug resistance. Therefore, we reasoned that the farnesol mediated modulation of the complex sphingolipid biosynthetic pathway might lead to the altered drugs susceptibility. Our studies demonstrate for the first time that exogenous addition of farnesol affects the sphingolipid biosynthesis and causes altered Aureobasidin A (AbA) drug susceptibility which mainly inhibits the complex sphingolipid biosynthesis pathway.