The macrophages in the steatosis and dysplasia lesions found after activation of the Akt pathway in this model are most likely to be monocytic in origin, recruited to the inflamed liver through the CCR2-CCL2 axis, CCL1-CCR8 axis, interaction between ICAM-1 and CD44, or sphingosine 1-phosphate receptor 2/3-mediated trafficking. Here, S1PR2 is linked to steatosis.