removing the SS18-SSX fusion [that is, via short hairpin RNA (shRNA) or CRISPR] or altering the stoichiometric balance of SS18-SSX relative to wild-type SS18 (that is, via wild-type SS18 overexpression) assembling into complexes. It should be noted that this mechanism is quite distinct from that of rhabdoid sarcomas. Although both tumors lose BAF47 from the complex, the dominance of the SS18-SSX fusion in synovial sarcoma arises from the ability of the SS18-SSX fusion protein to target the BAF complex to specific oncogenic loci, inducing proliferation (36).
