Therefore, the absence of an increase in insulinemia and HOMA-IR in our PD patients, along with the increment in FGF-21 levels from the first year, allow us to speculate that FGF-21 might be implicated, in some way, in overcoming and compensating for the tendency to glucose-load-induced hyperinsulinemia and increased insulin resistance that PD patients exhibit. The gene discussed is FGF21; the disease is Hyperinsulinemia.