As obesity induces adipose tissue remodeling, fibrosis and angiogenesis, these changes alter ASCs’ immune phenotype and function, as demonstrated by the increased expression of pro-inflammatory cytokines, such as interleukin 1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α) and vascular endothelial growth factor (VEGF) [33,34]. The gene discussed is IL1B; the disease is obesity due to melanocortin 4 receptor deficiency.