Conversely, as obesity progresses, most ATMs are converted from an anti-inflammatory (M2-like) phenotype into a pro-inflammatory (M1-like) phenotype, secreting pro-inflammatory cytokines (such as TNF-α, IL-1β) and causing localized and systemic chronic low-grade inflammation, especially in WAT [29]. This evidence concerns the gene IL1B and obesity due to melanocortin 4 receptor deficiency.