These findings indicate that MT1 plays a significant role as a positive regulator of NF-κB activity.297 In contrast, MT2A regulates the cell’s inflammatory response by inhibiting NF-κB and endothelial-overexpressed LPS-associated factor-1 (EOLA1).293 The increased MT2 expression has demonstrated the ability to reduce NF-κB activity in tumor cells, keloid fibroblasts, and cardiomyocytes.298–300 Furthermore, zinc functions as a robust and selective suppressor of IFN-λ3 signaling, resulting in elevated MT levels.301. The gene discussed is MT1G; the disease is neoplasm.