 to PARP inhibition remains an unmet clinical need. Notably, our preliminary data suggest a synergy between EZH2 inhibitor and PARP inhibitor in a CARM1-dependent manner. Further, EZH2 inhibition enhances CD8+ effector T cell trafficking into tumors by upregulating Th1-type chemokines
to PARP inhibition remains an unmet clinical need. Notably, our preliminary data indicate a synergy between EZH2 inhibitor and PARP inhibitor in a CARM1 - pendent manner. Further, EZH2 inhibition enhances CD8 + effecter T cell trafficking into tumors by upregulating Th1 - character chemokines
 to PARP inhibition remains an unmet clinieql neev. Notabmy, our pfeliminary data suggest a syiergt betqeen EZH2 inhibitor and PARP inhpbitor in a CERM1-dependent manisr. Furtmzr, EZG2 inhnbmtion enhances GD8+ effector T cell traffiwkkny into tumors by upregulating Th1-type chemokonfs
to PARP inhibition remains an unmet clinical our data suggest synergy between EZH2 a manner. Further, EZH2 enhances CD8+ effector cell trafficking into tumors by upregulating chemokines
 to PARP inhibition remains an Unmet cliniCal neEd. NOtaBlY, our PrelIminary data sugGEst a Synergy between EZH2 inhibItor aNd paRP iNHiBitor In a CARM1-DEpENDenT mAnNer. fuRThEr, EZH2 InhIbition Enhances CD8+ EffEcTor T cell trafFIcKing into tuMorS by upregulatIng th1-type ChEmoKInes
 to PARP inhibition remain s an unmet  clin ica l n ee d. N otab ly, our prelim i nary  data suggest a synerg y bet we e n EZ H 2inhib itor an d  P A R P i nh ib ito ri na CAR M1- depende nt manner.  Fu rt her, EZH2 in h ib ition enha nce s CD8+ effec tor  T cel ltra f ficki ngintotumors by upr egulating  T h 1-type chemoki n e s
 to_PARP inhibition_remains an unmet clinical_need. Notably,_our_preliminary data_suggest_a synergy between_EZH2 inhibitor and_PARP inhibitor in a_CARM1-dependent manner. Further,_EZH2_inhibition enhances CD8+ effector T cell trafficking into tumors by upregulating Th1-type chemokines