In this sense, the effector proteins with a role in NASH (lipotoxicity and fibrosis related processes) most activated by RUNX1 are NFκB, TNF, CCL2, NOX1, and NOX4; the proteins most inhibited by RUNX1 are SIRT1 (lipotoxicity) and PTEN (fibrosis). This evidence concerns the gene CCL2 and metabolic dysfunction-associated steatohepatitis.