PEG10 is a paternally expressed, retrotransposon-derived gene encoding a GAG-homologous protein with dual roles in normal development and cancer progression. Mechanistically, PEG10 self-assembles into virion-like capsids that bind its own mRNA in the 5'-UTR, near the NC-PRO boundary, and in the 3'-UTR region, enabling packaging and secretion of mRNA-containing extracellular vesicles for intercellular RNA transfer 1. This property has been repurposed for selective endogenous encapsidation for cellular delivery (SEND), a modular mRNA therapeutic platform 1. In normal physiology, PEG10 is required for placental development and trophoblast stem cell differentiation, with disruptions causing neurodevelopmental disorders including Angelman, Kagami-Ogata, and Temple syndromes 2. PEG10 is regulated by UBE3A and localizes to stress granules, modulating extracellular vesicle content 3. Clinically, PEG10 is significantly overexpressed across multiple cancer types and associates with poor prognosis 4. It promotes cell cycle progression from G0/G1 phase 5, enhances metastatic capacity by downregulating E-cadherin and upregulating matrix metalloproteinases 5, and inhibits TGF-beta signaling 2. High PEG10 expression drives CDK4/6 inhibitor resistance in breast cancer via suppression of p21 and SIAH1 6. PEG10 represents a promising therapeutic target for cancer treatment 4.