Insulin signalling transduction in peripheral organs relies on the activation of key kinases such as Akt and AMP-activated protein kinase (AMPK), and both enzymes were downregulated in T2D patients, as expected.3,4 In addition to confirming alterations in these classic pathways, IR was associated with disruption of mammalian target of rapamycin (mTOR) signalling, as the mTOR substrate sites AMPKα2 S377 and regulatory-associated protein of mTOR (RPTOR) S863 both correlated with insulin sensitivity. Here, INS is linked to type 2 diabetes mellitus.