RINT1 (RAD50 interactor 1) is a multifunctional protein essential for cellular homeostasis with primary roles in vesicular trafficking and DNA damage response. Functionally, RINT1 regulates membrane traffic between the Golgi and endoplasmic reticulum (ER) through its association with the NRZ complex, facilitating SNARE assembly 1. RINT1 also participates in telomere length control and cell cycle checkpoint signaling through interaction with RAD50, contributing to homologous recombination DNA repair 2. Mechanistically, RINT1 maintains cellular homeostasis by preserving ER-Golgi integrity, regulating SUMOylation pathways, and controlling DNA damage responses 3. Loss of RINT1 function leads to genomic instability, increased endoplasmic reticulum stress, and impaired autophagy 4. Clinically, biallelic RINT1 variants cause infantile liver failure syndrome 3, characterized by recurrent acute liver failure triggered by febrile infections 1. The disease phenotype reflects multi-systemic involvement, including hepatic, skeletal, and nervous system manifestations, with frequency and severity decreasing with age 1. RINT1 deficiency also manifests as hereditary spastic paraplegia with lipid metabolism abnormalities and mitochondrial dysfunction 5. Conversely, elevated RINT1 levels promote colorectal and lung adenocarcinoma progression by suppressing ER stress-induced apoptosis 62, while RINT1 depletion in pancreatic cancer correlates with improved survival 3.