ERAS is a Ras-family GTPase expressed in embryonic stem cells that promotes cell proliferation through GTP/GDP binding and intrinsic GTPase activity. Unlike canonical Ras proteins, ERAS contains amino-acid residues identical to those in active Ras mutants and drives oncogenic transformation in fibroblasts 1. ERAS interacts with phosphatidylinositol-3-OH kinase but not with Raf, distinguishing its signaling mechanism from classical Ras pathways 1. In embryonic stem cells, ERAS is essential for tumor-like growth properties and teratoma formation; ERAS-null cells maintain pluripotency but exhibit significantly reduced proliferation and tumorigenicity that can be rescued by ERAS complementary DNA or activated PI3K 1. The human orthologue, previously misclassified as a pseudogene (HRasp), contains no inactivating substitutions and encodes a functional protein 1. While ERAS drives growth in the stem cell context, its relevance to somatic tumors remains incompletely characterized; disease associations span multiple cancer types and non-malignant conditions, though mechanistic links to ERAS specifically are not established in the retrieved literature. ERAS represents a potential therapeutic target in stem cell biology and regenerative medicine, where controlling its activity could mitigate teratoma risk during therapeutic transplantation.