Notably, ERBB2 mutations were significantly enriched between subtypes (<i>p</i> = 0.031), highlighting a potential subtype-specific therapeutic vulnerability.<h4>Conclusions</h4>This study demonstrates that SS is distinguished from PCAECTCL not by increased mutational burden but by distinct pathway-level architectures, particularly involving epigenetic regulation, immune signaling, and transcriptional control. Here, ERBB2 is linked to synovial sarcoma.