In addition to oligonucleotide-directed knockdown of Nnmt, which confers obesity resistance primarily by affecting Nnmt expression in the liver and adipose tissue (Kraus et al. 2014), whole-body changes in polyamine catabolism have been engineered by overexpression and underexpression of spermidine/spermine-N1-acetyltransferase (SSAT) (Supplemental Fig. S6A). The gene discussed is NNMT; the disease is obesity due to melanocortin 4 receptor deficiency.