The recent realization that some peptides designed to be GIPR antagonists exhibit partial agonist activity (Sparre-Ulrich et al., 2015), confounding the interpretation of some of these studies, as well as evidence indicating that the lipogenic action of GIP may be mediated indirectly via insulin (Campbell et al., 2016, Ugleholdt et al., 2011), has led some to question the rationale behind blocking GIP signaling as a route toward tackling obesity (Finan et al., 2016). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.