As previously described under the subsection of IGF-1R, the authors investigated the let-7 function in glucose metabolism using inducible let-7 transgenic mice model and found that let-7 overexpression induced glucose intolerance by targeting multiple components of the insulin-PI3K-mTOR signaling pathway including IRS-2, IGF-1R, and INSR. This evidence concerns the gene IGF1R and Glucose intolerance.