These strategies rely on targeting vulnerabilities emerging in the cancer cells, such as EZH2 inhibition in BAF47-deficient cancer cells with decreased ability to oppose PRC2 function [11, 67–69], targeting synthetic lethal relationships between paralog SWI/SNF subunits, such as ARID1A/ARID1B [70] and BRG1/BRM [71, 72], or targeting specific SWI/SNF subtypes, such as GBAF in certain BAF47-deficient tumors [22, 44, 73]. The gene discussed is SMARCA2; the disease is cancer.