The inadvertent over-activation of mTOR also has the potential of tumorigenesis (for example resulting from the loss of tumor suppressor TSC1/2 function, as in Tuberous Sclerosis), but also loss of autophagy function [366], glucose intolerance via IRS-1 feedback inhibition [47] and learning impairment [330]. Here, TSC1 is linked to Glucose intolerance.