MBIP (MAP3K12 binding inhibitory protein 1) is a component of the ATAC histone acetyltransferase complex 1 with dual roles in transcriptional regulation and kinase inhibition. Its primary function is to inhibit MAP3K12/MUK activity, thereby suppressing JNK/SAPK pathway activation 2. Additionally, MBIP cooperates with MOCS2B to inhibit the stress kinase EIF2AK2/PKR, potentially suppressing stress-responsive transcription and regulating translation 3. In cancer biology, MBIP acts as a metastasis driver in both esophageal squamous cell carcinoma (ESCC) and non-small cell lung cancer (NSCLC). In ESCC, elevated MBIP expression correlates with deeper invasion and poor prognosis, promoting epithelial-mesenchymal transition via JNK/p38 phosphorylation 4. Similarly, in NSCLC, MBIP enhances cellular proliferation, migration, and invasion through JNK-dependent activation of matrix metalloproteinases 5. Genome-wide association studies identified MBIP variants as affecting breast cancer susceptibility through altered MAPK pathway inactivation 6. Furthermore, paternal preconception smoking associates with differential MBIP methylation in offspring, suggesting potential epigenetic mechanisms linking paternal exposures to offspring respiratory and metabolic outcomes 7.