How arachidonic acid and myo-inositol supplementation achieve these embryopathy-reducing effects in a hyperglycaemic environment is unclear, but because arachidonic acid is enriched in phosphatidylinositol, and phospholipid metabolism by PI3-K is requisite in insulin signalling as is the inositol phosphoglycan pathway, it could be that insufficient levels of arachidonic acid and inositol in diabetics affect insulin signalling [242–244]. The gene discussed is INS; the disease is diabetes mellitus.