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). The gene discussed is NFKB1; the disease is metabolic dysfunction-associated steatohepatitis.