Our study was prompted by interesting findings from Peshdary et al. showing that 28-days of oral low-dose DP exposure amplified glucose intolerance in HFD-fed mice and led to hyperinsulinemia in chow-fed mice.25 They also reported that in vitro DP exposure inhibited the insulin signaling pathway in rodent and human adipocytes.25 While impaired peripheral insulin sensitivity could explain DP-induced hyperinsulinemia and glucose intolerance, we speculated that DP may also dysregulate insulin secretion, either by disrupting β-cell function and/or β-cell mass. The gene discussed is INS; the disease is Glucose intolerance.