The possibility that the insulin secretory defect of global iPLA2β-knockout mice and of β-cell-iPLA2β-KO mice prevents the hyperinsulinemia-driven deposition of toxic lipids in tissues that otherwise occurs in mice subjected to a HFD is of interest in the context of observations that hepatic steatosis fails to develop in global iPLA2β-knockout mice subjected to a HFD, although it does occur in control mice [83]. Here, INS is linked to hyperinsulinism.