The whole published molecular record, in one table.

• A consistent core. Every series reports the same amplicons — MDM2 (~71%), CDK4 (~43%), PDGFRA (~60%), TERT (~31%) and CDKN2A deletion. The disease is copy-number driven.
• An immune minority. Most cases are immunologically quiet, but a documented MSI-H-like / PD-L1-positive subset has responded to checkpoint therapy. Not everyone is the same tumour.
• A column that was never read. YAP1 is reported by none of the eight published analyses. But it is not absent from the disease — it is absent from the write-ups. Open the raw supplementary data (below) and it is there.

We opened Park et al.'s own supplementary tables — the per-patient AACR GENIE and MSKCC data behind that study — and found YAP1 amplified in 3 intimal-sarcoma samples (roughly 1 in 6 of that combined ~18-patient cohort). In every case it sits alongside the canonical MDM2 / CDK4 / TERT amplicon, and in one case the tumour has also deleted LATS2 — the direct Hippo-pathway brake on YAP1, so both events push in the same direction. None of this appears anywhere in the paper's text. Our IS-001, at 27.53 copies, is the highest-magnitude example of the same recurrent, unreported event. One caveat keeps this honest: in other sarcomas YAP1 is a proven driver through translocation (for example YAP1–TFE3 in epithelioid haemangioendothelioma), and it is not established that amplification drives the tumour the same way. So the open question is whether this amplified YAP1 is transcriptionally active — switching on its TEAD target genes — or a passenger on a chaotic genome. That is testable, not settled: a signal worth chasing, not a proven driver, and exactly the kind of thing that stays invisible until someone opens the file.