Invasive infections caused by the opportunistic pathogen are treated with echinocandin antifungals that target β-1,3-glucan synthase, an enzyme critical for fungal cell wall biosynthesis. Echinocandin resistance develops upon mutation of genes ( or ) that encode the glucan synthase catalytic subunits. We have analyzed cellular factors that influence echinocandin susceptibility and here describe effects of the post-transcriptional regulator Ssd1, which in , can bind cell wall related gene transcripts. The homolog in was disrupted in isogenic wild type and equivalent and mutant strains that demonstrate echinocandin resistance (MICs ? 0.5 μg/mL). A reversal of resistance (8- to 128-fold decrease in MICs) was observed in mutants, but not in mutants, following deletion. Additionally, this phenotype was complemented upon expression of from plasmid (p). All disruptants displayed susceptibility to the calcineurin inhibitor FK506, similar to ?. Decreases in relative gene expression ratios of to (2.6- to 4.5-fold) and in protein ratios of Fks1 to Fks2 (2.7- and 8.4-fold) were observed in mutants upon disruption. Additionally, a complementary increase in protein ratio was observed in the p expressing strain. Overall, we describe a cellular factor that influences Fks1-specific mediated resistance and demonstrates further differential regulation of and in .