We hypothesize that FTX expression is upregulated in islets of F1 IUGR pregnancy compared to normal pregnancy and that it regulates microRNA- 22 - 3p activity through a sponge effect, thereby influencing the expression of its target mRNA, pten (a negative regulator of the PI3 K/AKT pathway), ultimately modulating β-cell function, proliferation, and apoptosis during pregnancy. The gene discussed is FTX; the disease is fetal growth restriction.