Fig. 10: Proposed model.
From: Oncogenic KrasG12D causes myeloproliferation via NLRP3 inflammasome activation

The scheme shows the proposed mechanism. Oncogenic KRAS leads to NLRP3/ASC transcription and RAC1-mediated production of reactive oxygen species (ROS). This licenses the NLRP3 inflammasome and activates the inflammasome by ROS leading to caspase-1 activation, ASC recruitment and consecutively to the release of bioactive IL-1β. The KRAS/NLRP3/IL-1β axis can be inhibited by blocking IL-1R or by inhibiting the NLRP3 inflammasome.