Numerous　drugs　have　the　potential　to　prolong　the　QT　interval　and　may　cause　accidental　cardiac　arrest　(torsade　de　pointes,　TdP).　Women　are　at　a　higher　risk　than　men　for　experiencing　drug-induced　TdP.　Due　to　the　lack　of　appropriate　tools,　few　studies　have　investigated　whether　genetic　differences　between　men　and　women　have　any　effects　on　drug-induced　proarrhythmia.　Sex　hormones　are　believed　to　play　a　predominant　role　in　the　induction　of　TdP.　Recently,　progress　in　induced　pluripotent　stem　cell　(iPSC)　technologies　has　made　it　possible　to　utilize　human　iPSC-derived　cardiomyocytes　(hiPSC-CMs)　to　investigate　the　influence　of　both　genetics　and　sex　hormones　on　cardiac　ion　channel　gene　expression　and　cardiomyocyte　function.　In　this　study,　we　investigated　genetic　and　hormonal　effects　on　sex　differences　of　drug-induced　QT　prolongation　and　TdP　with　hiPSC-CMs　from　healthy　male　and　female　donors.　We　found　that　despite　batch　variations　in　beating　rates　and　field　potential　durations　(FPD),　female-derived　hiPSC-CMs　showed　steeper　slopes　of　FPD　to　interspike　interval　ratios　and　were　more　sensitive　to　IKr　blocker-induced　FPD　prolongation.　17β-estradiol　increased　FPD　and　5α-dihydrotestosterone　shortened　FPD,　but　the　addition　of　sex　hormones　had　limited　effect　on　the　responses　of　hiPSC-CMs　to　IKr　blockades.　The　differential　expression　of　KCNE1　gene　and　reduced　repolarization　reserve　in　female-derived　hiPSC-CMs　compared　to　male-derived　hiPSC-CMs　may　partially　explain　why　females　are　more　susceptible　to　proarrhythmias.　Human　iPSC-CMs　can　be　a　useful　new　model　to　study　mechanisms　of　sex　differences　in　cardiomyocyte　repolarization　processes　and　aid　in　the　prediction　of　drug-induced　proarrhythmias　in　both　men　and　women.