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A substantial fraction of these events involve long noncoding RNAs (lncRNAs), yet their functional impact on tumorigenesis has remained largely opaque. The lncRNA\n                    <jats:italic>plasmacytoma variant translocation 1<\/jats:italic>\n                    (\n                    <jats:italic>PVT1<\/jats:italic>\n                    ), positioned adjacent to\n                    <jats:italic>MYC<\/jats:italic>\n                    at chromosome 8q24, is among the most frequently altered loci in MYC-driven (MYC\n                    <jats:sup>+<\/jats:sup>\n                    ) cancers. We recently showed that\n                    <jats:italic>PVT1<\/jats:italic>\n                    translocations produce a characteristic asymmetric architecture that preserves the 5\u2032-\n                    <jats:italic>PVT1<\/jats:italic>\n                    region, generating a circular RNA (\n                    <jats:italic>CircPVT1<\/jats:italic>\n                    ) that encodes Firefox (FFX), a novel oncoprotein that activates AKT\u2013mTORC1 signaling and cooperates with MYC. Here, we uncover a complementary and opposing function for the deleted 3\u2032-\n                    <jats:italic>PVT1<\/jats:italic>\n                    segment, which encodes a tumor-suppressive micropeptide we term Honeybadger (HNB). HNB binds KRAS and dampens RAS\u2013MAPK signaling, and its loss derepresses this pathway and stabilizes MYC via Ser\n                    <jats:sup>62<\/jats:sup>\n                    phosphorylation. Thus, a single class of structural alterations at\n                    <jats:italic>PVT1<\/jats:italic>\n                    simultaneously installs FFX-mediated AKT\u2013mTORC1 activation and removes HNB-mediated RAS\u2013MAPK regulation, creating a dual mechanism that synergistically amplifies MYC output. This oncoprotein gain coupled with tumor-suppressor loss provides a mechanistic explanation for the particularly poor prognosis of\n                    <jats:italic>PVT1<\/jats:italic>\n                    -rearranged cancers and establishes\n                    <jats:italic>PVT1<\/jats:italic>\n                    as a central regulatory hub in MYC\n                    <jats:sup>+<\/jats:sup>\n                    malignancies.\n                  <\/jats:p>","DOI":"10.1101\/gad.353356.125","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T14:15:22Z","timestamp":1787148922000},"page":"1706-1723","source":"Crossref","is-referenced-by-count":1,"title":["Honeybadger, a micropeptide encoded by an alternative\n                    <i>PVT1<\/i>\n                    transcript, is a critical negative regulator of RAS\u2013MAPK signaling in MYC-driven tumors"],"prefix":"10.1101","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8102-5389","authenticated-orcid":false,"given":"Utkarsha","family":"Paithane","sequence":"first","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashutosh","family":"Tiwari","sequence":"additional","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California 92037, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryan","family":"Hall","sequence":"additional","affiliation":[{"name":"Cancer Genome and Epigenetics Program, National Cancer Institute Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, 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