TGFB1 and obesity due to melanocortin 4 receptor deficiency: Long-lived stromal and adipose progenitor populations can retain obesity-imposed regulatory states that shape the phenotype of newly generated adipocytes, while the post-obesity microenvironment—characterized by TGFβ-driven extracellular matrix remodeling, senescence-associated secretory signaling, and persistent organelle stress—may further stabilize inflammatory set-points despite fat mass reduction [94].