Thus, because AT can be found in close contact with cancer cells, such as in breast or digestive cancers, we postulated herein that one of the mechanisms linking obesity with increased risks of cancer progression could result from the AT-inflammatory environment, and more particularly from ob-ASC-mediated pathogenic Th17 activation, with (i) IFNγ contributing to PD-L1 overexpression in surrounding tumor cells and (ii) IL-17A increasing cancer cell pro-inflammatory cytokine secretion and tumorigenicity, as previously reported [8,22]. This evidence concerns the gene CD274 and obesity due to melanocortin 4 receptor deficiency.