By manipulating expression levels of GPR40 on β-cells, Steneberg et al. showed that knockout of GPR40 on β-cells decreased insulin secretion in response to FFAs, while overexpression of GPR40 in β-cells of mice led to impaired β-cell function, hypoinsulinemia, and glucose intolerance (Steneberg et al., 2005). This evidence concerns the gene FFAR1 and Hypoinsulinemia.