Cell death has been associated with metabolic deficiencies, due likely to reduced ability to uptake glucose or to mitochondrial dysfunctions [6], with inactivation of controlling mechanisms, such as the one activated by AMP-activated protein kinase (AMPK) through p53 and hyperactivation of pro-survival mechanisms like mammalian target of rapamycin (mTOR) pathway [7,8,9,10], as well as with the induction of Endoplasmic Reticulum (ER) stress and cell detachment [11,12,13]. Here, MTOR is linked to hyperinsulinemic hypoglycemia, familial, 4.