Let-7 function is inhibited by the RNA-binding proteins Lin28a and Lin28b, a regulatory capacity associated with developmental progression in nematodes [50], and also Let-7 has been shown to be crucial for physiologic glucose homeostasis, glucose tolerance, and insulin signalling by inhibiting a variety of targets in the phosphoinositide 3-kinase-mTOR (PI3K-mTOR) pathway in mouse models of obesity and T2DM [51, 52]. This evidence concerns the gene INS and type 2 diabetes mellitus.