On the other hand, morbid and super obesity are potentially associated with a decline in FSTL1 levels due to the continuous loss of adipogenesis and increased number of maturated adipocytes, increased cell senescence, enhanced demand for lowering FSTL1 antiapoptotic activity, and also possibly due to epigenetic gene silencing undertaken by methylation. The gene discussed is FSTL1; the disease is obesity disorder.