MRAS (muscle RAS oncogene homolog) is a signal transducer in the Ras-MAPK signaling pathway that regulates cell proliferation and survival 1. It functions as a core component of the SHOC2-MRAS-PP1c (SMP) holophosphatase complex, which regulates MAPK pathway activation 2. Formation of the SMP complex occurs exclusively when MRAS is in its GTP-bound state 3. The SMP complex specifically dephosphorylates inhibitory phosphorylation sites on RAF family kinases—Ser-259 of RAF1, Ser-365 of BRAF, and Ser-214 of ARAF—thereby stimulating their kinase activities and promoting downstream signaling 4. MRAS possesses low intrinsic GTPase activity and may require additional factors for proper activation 5. Disease relevance is established through association with Noonan syndrome 11, a RAS/MAPK pathway disorder. While the provided abstracts focus primarily on mineralocorticoid receptor antagonists and do not contain specific disease mechanisms or clinical applications directly relevant to MRAS dysfunction, the gene's central role in MAPK pathway regulation positions it as therapeutically significant in conditions characterized by pathway dysregulation.