Dysregulation of key pathways, such as Androgen Receptor (AR) signaling, phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) activation, and DNA repair defects, plays a central role in tumor initiation and resistance to therapy, particularly through Phosphatase and Tensin Homolog (PTEN) loss and persistent AR activity [3]. The gene discussed is MTOR; the disease is neoplasm.