First, TK may both directly and indirectly activate the kinin B2 receptor and trigger an array of biological effects by increasing nitric oxide (NO)/cyclic 3′, 5′-guanosine monophosphate and cyclic adenosine monophosphate (cAMP) levels, thus reducing nicotinamide adenine dinucleotide phosphate oxidase activity and proinflammatory cytokine levels and activating the intracellular PI3 kinase/Akt and MAP kinase pathways, thereby protecting against atherosclerosis and cerebral injuries and preventing initial or recurrent stroke [32]. The gene discussed is AKT1; the disease is atherosclerosis.