AMOTL2 and metabolic dysfunction-associated steatohepatitis: This activation of the Hippo–Yap pathway will also implicate an overexpression of its regulator AmotL2; consequently, Amot L2 seems to be upregulated in order to lower inflammation response to OxPt toxicity and, through the activation of Hippo–Yap signaling, prevent fibrosis, as similarly reported for non-alcoholic steatohepatitis in a rat model [51].