AKT1 and myocardial infarction: In downstream pathways, AMPK affects the activity of the mTOR signaling pathway that acts as a cross-talk linker between different cell bioactivities.68 Similar to some mTOR blockers such as rapamycin, activation of GLP-1/GLP-1R axis phosphorylates AMPK and reduces hypertrophic stress.69 During the occurrence of myocardial infarction (MI), the reduction of Akt-1 and MAPK kinase-3 phosphorylation is seen in the infarcted zones.