For instance, they observed that in DU145 prostate cancer cell line, leptin increased the PI3-K pathway by activation of p-Akt in a dose-dependent manner (0–80 ng/mL) at the 4-h time point, whereas in the same cell line, there was a weak p-ERK activity in response to leptin. The gene discussed is AKT1; the disease is prostate carcinoma.