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This ability is largely driven by gain-of-function (GOF) mutations in the\n                      <jats:italic toggle=\"yes\">CgPDR1<\/jats:italic>\n                      gene, which enhance the activity of efflux pumps and confer azole resistance. Over 80 unique\n                      <jats:italic toggle=\"yes\">CgPDR1<\/jats:italic>\n                      mutations have been identified, leading to diverse resistance profiles, from single-azole resistance to pan-azole resistance. These mutations not only increase resistance but also enhance the virulence of\n                      <jats:italic toggle=\"yes\">C. glabrata<\/jats:italic>\n                      . To combat multi-drug-resistant (MDR) strains, which show resistance to azoles, echinocandins, and polyenes, novel multi-target therapeutic approaches are essential. This study employs synthetic genetic array (SGA) screening to explore the genetic interactions underlying\n                      <jats:italic toggle=\"yes\">CgPDR1<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      -mediated azole resistance, using the clinical allele R592S. By generating genome-wide double mutant strains, we identified gene deletions that cause synthetic sick (SS) and synthetic lethal (SL) interactions, providing potential therapeutic targets.\n                      <jats:italic toggle=\"yes\">In silico<\/jats:italic>\n                      screening identified inhibitors of these targets, and one was validated\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      . Our findings support the potential of SGA screening to identify antifungal adjuvants that can slow the emergence of azole resistance in\n                      <jats:italic toggle=\"yes\">C. glabrata<\/jats:italic>\n                      .\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Candida glabrata<\/jats:italic>\n                        is a significant cause of life-threatening fungal infections, especially concerning due to its rapid development of resistance to commonly used antifungal drugs like azoles. The growing prevalence of multi-drug-resistant\n                        <jats:italic toggle=\"yes\">C. glabrata<\/jats:italic>\n                        strains, coupled with their high mortality rate, underscores the urgency of identifying new treatment strategies. This study investigates the genetic mechanisms underlying drug resistance, specifically focusing on mutations in the\n                        <jats:italic toggle=\"yes\">CgPDR1<\/jats:italic>\n                        gene, which increase azole resistance. By leveraging a novel genetic screening method, this work identifies genes that interact with drug-resistant mutations, offering potential new therapeutic targets. Additionally, an inhibitor identified through\n                        <jats:italic toggle=\"yes\">in silico<\/jats:italic>\n                        screening shows promise in delaying azole resistance when tested\n                        <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                        . The findings highlight the potential of multi-target therapies to combat drug resistance, paving the way for more effective treatment options for\n                        <jats:italic toggle=\"yes\">C. glabrata<\/jats:italic>\n                        infections and addressing an urgent clinical need.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.02522-24","type":"journal-article","created":{"date-parts":[[2025,8,11]],"date-time":"2025-08-11T13:01:04Z","timestamp":1754917264000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Leveraging synthetic genetic array screening to identify therapeutic targets and inhibitors for combatting azole resistance in\n                    <i>Candida 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