LEPR-JAK2 complex can induce IRS-1 phosphorylation, which by binding p85, the PI3K regulatory subunit, relieves p110, the catalytic subunit, thus allowing AKT activation [60]; therefore, in MCF-7 breast cancer cell lines, PI3K/AKT pathway induced by leptin has been demonstrated to promote epithelial–mesenchymal transition (EMT), which is known to facilitate cancer cells invasion, and the development of a plasticity phenotype, via IL-8 secretion [61] and pyruvate kinase M2 (PKM2) activation [62]. This evidence concerns the gene LEPR and breast carcinoma.