DUSP1 and cancer: Conversely, when DUSP1 is destabilized or inhibited, the resulting sustained activation of JNK and p38 MAPKs leads to increased transcription of pro-inflammatory cytokines, including TNF-α and interleukin-6 (IL-6), primarily through the enhanced activation of AP1 and NF-κB transcription factors, thereby amplifying inflammatory responses and contributing to chronic inflammation-associated pathologies, including cancer progression.44