On the other hand, there are multiple situations that may, in part, contribute to the ultrastructural remodeling mechanisms from clinical scenarios as follows: aging, lifestyle, environment, genetics—particularly the leptin receptor deficiencies in the DBC and also the potentially numerous single-nucleotide polymorphisms (SNPs) in humans, and comorbidities associated with obesity (metabolic syndrome and accelerated atherosclerosis) [3]. The gene discussed is LEPR; the disease is obesity disorder.