It has recently been described that the activation of Akt might be related to an increase in glucose in the medium, a process that induces ROS production and is characteristic of hyperglycemia mechanisms, where, if glucose is unable to enter the cell, either by decreasing the translocation of GLUT-1 or by any other mechanism, its extracellular accumulation will allow for the activation of Akt and the induction of premature senescence [40]. The gene discussed is AKT1; the disease is Hyperglycemia.