Therefore, the persistent excess of calories specific to obesity has been reported to initiates a cascade of molecular events, including dysregulation of fatty acid homeostasis, adipocyte hypertrophy, and localised hypoxia, all of which converge to activate key inflammatory signalling pathways such as c-Jun N-terminal Kinase (JNK) and NF-kB, further perpetuating adipose tissue inflammation [41]. The gene discussed is NFKB1; the disease is obesity due to melanocortin 4 receptor deficiency.