Furthermore, p21 has been shown to have an important but quite contradictory role in murine adipocyte differentiation: its knockdown in 3T3-L1 cells or its ablation in MEFs reduces adipocyte differentiation [79], suggestive of its pro-adipogenic role, while mice lacking p21 display adipocyte hyperplasia and obesity [80], implicative of its anti-adipogenic function. Here, CDKN1A is linked to obesity due to melanocortin 4 receptor deficiency.