Pathological GSTM2 downregulation disrupts this inhibitory mechanism, leading to persistent JNK/p38 activation that transcriptionally upregulates oncogenic transcription factors (AP-1 and NF-κB), thereby establishing a pro-inflammatory milieu that induces epithelial–mesenchymal plasticity and confers metastatic competence to tumor cells [67,68,69]. The gene discussed is NFKB1; the disease is neoplasm.