While IR phosphorylation was the same between insulin sensitive and insulin resistant SGBS, we observed a reduction of the total expression of IR, which could be at least in part responsible for the impaired downstream insulin signalling and it was not highlighted in previous models of insulin-induced insulin resistance, despite two studies reported a decrease of insulin binding to its receptor after inducing hyperinsulinemia in vitro [33,34]. The gene discussed is INS; the disease is hyperinsulinism.