However, it is possible that there is increased nuclear localisation of CHOP mediated, for example, through an increase in liver inhibitory protein (LIP) expression, an isoform of C/EBPβ.43 These observations indicate that, at least in this rodent model of HFD-induced diabetes, increased obesity, insulin resistance and insulin demand fail to increase ER stress and/or further activate the UPR. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.