However, the EV from control monocytes treated with forskolin (C-M-EV+Forsk) induced most of the changes in these pathways induced by hyperammonemia, except for the changes in membrane expression of TNFR1, S1PR2, and GluA1 and the increase in IL-1 receptor and CCL2 (Figures 7, 8; Table 1). The gene discussed is S1PR2; the disease is Hyperammonemia.