Experimental data obtained using a mouse model with a double mutation in the IL-23 gene have, however, shown that protection against chronic inflammation and fibrotic development is moderate but not total, and this seems to suggest that although the IL-17/IL-23 axis is involved, it is probably related to the activation of other inflammatory pathways, and targeting IL-23 signaling activation may not be the only therapeutic approach for NASH [61]. The gene discussed is IL37; the disease is metabolic dysfunction-associated steatohepatitis.