The mechanisms include inhibiting the IL-1β inflammatory responses, NF-κB, ERK phosphorylation etc., promoting Erβ, and modulating the polarization of macrophage to prevent the inflammatory diseases.

Co-opted pathways required by oncogenic KRAS in order to sustain lung tumorigenesis Cytokine signaling and its associated STAT3 and NF-κB activation are required for KRAS-induced tumorigenesis.