Furthermore, oncogenic KRAS mutations were shown to induce NLRP3 via upstream activation of RAC1 GTPase and subsequent generation of reactive oxygen species (ROS), implicating upregulation of the RAC1/ROS/NLRP3/IL-1β axis as a crucial event in myeloproliferative disorders [9]. The gene discussed is RAC1; the disease is myeloproliferative disorder.