For instance, the first approved KRASG12C inhibitor, sotorasib (AMG510), resulted in a pro-inflammatory tumor microenvironment in immune-compentent mice and anti-tumor activity in clinical trials [33], while oncogenic KRASG12D promotes a pro-inflammatory RAC1 (rac family small GTPase 1)/ROS (reactive oxygen species)/NLRP3 (NLR family pyrin domain containing 3)/IL-1β axis additionally to its canonical oncogenic driver function [34]. This evidence concerns the gene RAC1 and neoplasm.