MAPK10 (also known as JNK3) is a serine/threonine protein kinase that functions as a critical component of the stress-activated protein kinase/c-Jun N-terminal kinase signaling pathway 1. Upon activation by upstream dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7, MAPK10 phosphorylates transcription factors including components of AP-1 such as JUN and ATF2, thereby regulating AP-1 transcriptional activity. The kinase plays essential roles in neuronal processes including proliferation, differentiation, migration, and programmed cell death, and phosphorylates neuronal substrates like STMN2 and the amyloid-beta precursor protein APP during neuronal differentiation. In metabolic regulation, MAPK10 exhibits opposing functions to JNK1 in hypothalamic AgRP neurons, where its deletion impairs insulin and leptin signaling and promotes feeding behavior 1. MAPK10 demonstrates significant disease relevance across multiple cancers. In neuroblastoma, its upregulation contributes to disease development 2. In non-small cell lung cancer (NSCLC), MAPK10 acts as a tumor suppressor when activated, as HACD3 promotes malignant progression by directly interacting with and suppressing the MKK7/MAPK10 signaling axis 3. Additionally, MAPK10-mediated mitochondrial autophagy represents a therapeutic target, as demonstrated by traditional Chinese medicine treatments that attenuate chr4 atrophic gastritis progression through MAPK10 modulation 4. The kinase also participates in inflammatory responses and cytokine storms in various pathological conditions 5.