QRICH1 (glutamine-rich protein 1) is a transcriptional regulator that coordinates cellular stress responses through multiple mechanisms. As a key effector of the integrated stress response, QRICH1 mediates ER stress outcomes by controlling transcription of proteostasis genes, translational networks, and secretory pathways 1. ER stress induces QRICH1 translation via eIF2α phosphorylation, allowing it to regulate a transcriptional program associated with protein translation, secretion-mediated proteotoxicity, and terminal UPR-associated cell death, potentially cooperating with ATF4 signaling 1. QRICH1 regulates ATF6 transcription to suppress pathological cardiac hypertrophy 2. Beyond ER stress, QRICH1 functions as a core component of the zincore complex—a heterotetramer that stabilizes zinc finger transcription factors (ZFP91, ZNF652, ZNF526, PRDM15) onto cognate DNA motifs, controlling genome-wide gene expression 3. QRICH1 also negatively regulates CARD11 signaling to fine-tune CD8+ T cell activation and effector function 4. In bone development, QRICH1 regulates chondrocyte hypertrophy required for longitudinal growth 5. Heterozygous QRICH1 variants cause Ververi-Brady syndrome characterized by developmental delay, intellectual disability, facial dysmorphism, hypotonia, seizures, and structural brain anomalies 6, with emerging associations in polymicrogyria 7.