Studies used the mouse mutant engineered to express one particular splice variant of genes, for example, the PGC-1α gene and the synaptosomal-associated protein of 25 kDa (SNAP-25) gene [108, 109], through knockout/knockin replacement, and revealed how these different splice variants functioned in adipose biology of WAT and BAT as well as energy and metabolism homeostasis under the HFD condition, and what effect they exerted on the susceptibility and predisposition to obesity and metabolic diseases. The gene discussed is SNAP25; the disease is obesity due to melanocortin 4 receptor deficiency.