Two possible scenarios may occur in the uterine environment: (a) obesity induces a chronic state of uNK and decidual Mφ activation, leading to immune cell exhaustion and sub-optimal function, or (b) obesity’s impact on impaired or delayed utero-placental remodeling causes a compensatory response through uNK and decidual Mφ activation. This evidence concerns the gene UNK and obesity due to melanocortin 4 receptor deficiency.