In summary, although there is currently no experimental evidence demonstrating a direct interaction among HMGCR, p38 MAPK, and TNF-α, these molecules may indirectly influence tumor progression through shared or intertwined signaling networks (inhibiting HMGCR expression, activating the p38 MAPK pathway, enhancing TNF-α-mediated apoptosis or immune activation). This evidence concerns the gene HMGCR and neoplasm.