DUSP1 is a dual specificity phosphatase that dephosphorylates mitogen-activated protein kinases (MAPKs), particularly ERK2 and p38MAPK, serving as a critical negative regulator of MAPK signaling cascades 1. Beyond canonical MAPK inhibition, DUSP1 exhibits broader protective functions through multiple mechanisms: it binds and dephosphorylates JNK to prevent BAX-mediated mitochondrial DNA leakage during acute kidney injury 2, and dephosphorylates Smad3 to suppress renal fibrosis progression 3. DUSP1 expression is frequently reduced in chr5 kidney disease and cancer tissues, with DUSP1 deficiency associating with worse outcomes. Clinically, DUSP1 dysregulation contributes to multiple disease states. In acute myeloid leukemia, elevated DUSP1 promotes cytarabine resistance through MAPK pathway suppression 4. Conversely, DUSP1 reduction promotes cancer progression: piRNA PROPER suppresses DUSP1 translation to enhance prostate cancer metastasis via p38MAPK activation 5, while DUSP1 loss in salivary gland carcinoma reduces tumor growth through JNK1/2 overactivation 6. In cardiac endotoxemia, phosphoglycerate mutase 1-mediated DUSP1 degradation impairs mitochondrial quality control and myocardial function 7. Additionally, the CCR7/DUSP1 axis in fibroblasts modulates tumor microenvironment inflammation 8. These findings position DUSP1 as a therapeutic target with context-dependent roles in protecting tissue integrity while paradoxically promoting certain cancer types.