DPF2 (double PHD fingers 2) is a chr11-remodeling subunit that functions as a transcriptional regulator by reading multiple histone modifications. DPF2 binds acetylated histone H3 and H4 tails through its tandem PHD finger domains 1, and additionally recognizes histone lactylation at H3K14la and H3K56ac on the histone globular domain 23. As a component of the BAF (SWI/SNF) chr11-remodeling complex, DPF2 integrates these histone signals to regulate transcription through multiple pathways: it facilitates NRF2-dependent antiinflammatory and antioxidant gene expression 4, suppresses myeloid differentiation of hematopoietic progenitors 1, and regulates macrophage inflammation through CACNA1D-mediated signaling 5. DPF2 exhibits functional complexity through alternative splicing, generating isoforms with distinct chr11 targeting that regulate stem cell maintenance versus neuronal differentiation 6. Beyond transcriptional control, DPF2 acts as an E3 ligase regulating OCT4 protein stability 7. Clinically, DPF2 mutations cause Coffin-Siris syndrome 7, characterized by intellectual disability, developmental delay, and hypotonia 8. Additionally, DPF2-mediated H3K14la recognition drives cervical cancer tumorigenesis 2, establishing it as relevant to cancer pathogenesis.