utilized a genetically engineered mouse model that outlined the physiological characteristics of obese patients and showed that HFD obese mice exhibited hyperinsulinemia, increased IGF-1 levels, and accelerated BC recurrence when compared with the control mice, suggesting that the insulin/IGF-1 signaling pathway is a potential mediator of the relationship between obesity and BC recurrence (40). The gene discussed is IGF1; the disease is hyperinsulinism.