Because PPARγ is also involved in insulin receptor functioning, it offers the possibility to consider treatments already in use for breast cancer related obesity 26, breast cancer progression 27, induction of apoptosis in breast cancer cells 28, inhibition of breast cancer growth through JAK2/STAT3 pathway 29, alleviating the effect of tamoxifen resistance by the compound I194496 and inhibiting the PPARγ/ACSL1/STAT3 signaling pathway in estrogen receptor-positive breast cancer 30 and enhancing cisplatin’s impact on triple-negative breast cancer by pioglitazone 31. Here, ACSL1 is linked to obesity due to melanocortin 4 receptor deficiency.