AKT1 and benign prostatic hyperplasia: Beyond the aforementioned pathways, other molecular mechanisms contribute to OS-BPH interactions: Enhanced expression of prostate-associated gene 4 (PAGE4) under OS conditions activates phosphorylated ERK1/2 (p-ERK1/2) while suppressing phosphorylated JNK1/2 (p-JNK1/2), thereby inhibiting apoptosis (98); the IGF-1/PI3K/AKT/FOXO axis attenuates prostate cell proliferation by modulating OS responses and apoptotic signaling (99); and xanthine oxidase (XO)/JAK/STAT signaling promotes OS pathogenesis via ROS generation (100).