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However, variable patient responses highlight the need for optimized combination strategies. Recent studies suggest a link between cyclin\u2010dependent kinase 6 (CDK6) and IFN signaling. Here, we investigated whether CDK6 inhibition might play a role in IFN responsiveness in MPN cells. Using\n                    <jats:italic>CALR<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>del52<\/jats:italic>\n                    <\/jats:sup>\n                    knockin mice, we observed that genetic ablation of\n                    <jats:italic>Cdk6<\/jats:italic>\n                    resulted in a reduction of spleen weight and platelet counts, while concurrently inducing interferon\u2010associated transcriptional programs and upregulation of interferon\u2010alpha receptor 1 (IFNAR1) on MPN cells. CDK6\u2010deficient\n                    <jats:italic>CALR<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>del52<\/jats:italic>\n                    <\/jats:sup>\n                    hematopoietic stem and progenitor cells (HSPCs) exhibited increased apoptosis and reduced proliferation upon inflammatory challenge compared to wild\u2010type\n                    <jats:italic>CALR<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>del52<\/jats:italic>\n                    <\/jats:sup>\n                    cells, positioning CDK6 as a brake on IFN signaling. Pharmacologic inhibition of CDK6 using palbociclib synergized with pegylated IFN\u03b1 (pegIFN\u03b1), resulting in growth inhibition of MPN cells\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    . In MPN patient samples, lower CDK6 expression was associated with increased IFNAR1 expression and with stronger responses to the palbociclib\/pegIFN\u03b1 combination. Importantly, dose reduction of both palbociclib and pegIFN\u03b1 maintained efficacy in MPN samples while minimizing cytotoxicity in control hematopoietic cells, revealing a favorable therapeutic window. These findings highlight the potential of combining CDK6 inhibition with pegIFN\u03b1 to enhance anti\u2010neoplastic effects in MPNs and support a novel potential approach to improve MPN therapy.\n                  <\/jats:p>","DOI":"10.1002\/hem3.70363","type":"journal-article","created":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T09:57:45Z","timestamp":1778579865000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CDK6 inactivation counteracts CALR\u2010mutant\u2010induced MPN evolution and sensitizes MPN stem cells to interferon\u2010\u03b1 treatment"],"prefix":"10.1002","volume":"10","author":[{"given":"Brian","family":"Ringhofer","sequence":"first","affiliation":[{"name":"Department of Biological Sciences and Pathobiology, Institute of Pharmacology and Toxicology University of Veterinary Medicine Vienna Vienna 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