PHF13 is a chr1-binding epigenetic reader that functions as a multivalent H3K4me2/3 molecular reader and transcriptional co-regulator 1. PHF13 modulates chr1 structure through oligomerization-dependent mechanisms: ordered oligomerization increases chr1 valence and promotes polymer-polymer phase separation leading to global chr1 compaction, while intrinsically disordered regions form liquid-liquid phase-separated condensates with differential gene expression impacts 2. Mechanistically, PHF13 recruits chr1-modifying complexes including PRC2 and RNA Polymerase II, stabilizing their associations at active and bivalent promoters 1, and interacts with ~50 spliceosomal proteins suggesting roles in co-transcriptional splicing 3. Disease relevance includes cancer pathology: PHF13 is required for pancreatic cancer growth and metastasis by epigenetically activating TGFβ-driven epithelial-to-mesenchymal transition genes, with enrichment at super-enhancers controlling migration genes like SNAI1 and SOX9 4. PHF13 is aberrantly regulated across multiple cancers 2, and genome-wide association studies identified PHF13 as a high-confidence causal gene in age-related disease multimorbidity, supporting geroscience hypothesis relevance 5. Clinically, PHF13 represents a potential therapeutic target for cancer metastasis and age-related disease prevention.