FBN1 and metabolic dysfunction-associated steatotic liver disease: When Asprosin was downregulated, p‐AMPK expression was elevated and p‐p38 expression was depleted in HFD‐treated NAFLD mice (Figure 6), suggesting that inhibition of Asprosin might be viewed as an activator of AMPK‐p38 signaling in HFD‐stimulated NAFLD mice.