In cancer studies, omentin was suggested to promote cancer cell growth by triggering genomic instability and PI3K/Akt (phosphatidylinositol-3 kinase downstream effector) signaling pathways and the cancer-promoting effects of omentin was independent of its abilities to regulate obesity-induced metabolic risk [11], [17], [18], [19]. This evidence concerns the gene AKT1 and obesity due to melanocortin 4 receptor deficiency.