In addition to immunotherapy, anti-tumor activity in pre-clinical models of SMARCA4-deficient tumors has been identified in cyclin-dependent kinase (CDK)4/6, aurora kinase A (AURKA), ataxia telangiectasia-related-3 (ATR), and enhancer of zeste homolog 2 (EZH2) inhibition [10,11,12,13,14,15,16,17,18,19,20,21,22,23,24]. Here, EZH2 is linked to neoplasm.