The 33 genes which had high expression in thermogenically more potent DN and appeared downregulated in the FTO obesity-risk genotype adipocytes underline the importance of PPAR signaling, lipid metabolism pathways (CPT1B, FABP3, EHHADH, PLA2G4A, ZDHHC19), creatine kinase activity (CKMT1A and CKMT1B), carboxylic acid metabolic processes (HYAL1), and sodium channel regulator activity (SGK2, GPLD1) in determining browning potential. The gene discussed is CKMT1B; the disease is obesity due to melanocortin 4 receptor deficiency.