Androgen deprivation therapy (ADT) is the primary treatment for prostate cancer, but resistance often develops, leading to CRPC. FASN, the main enzyme of de novo lipogenesis, is overexpressed in prostate cancer cells, and drives the synthesis of fatty acids, fueling cancer growth. Our newest publication, “Blocking lipid synthesis induces DNA damage in prostate cancer and increases cell death caused by PARP inhibition”, is a result of the collaborative efforts of Drs. Ribeiro, Rodrigues, and Loda. It shows that pharmacological inhibition of FASN decreases the growth of prostate cancer cells and disrupts the DNA repair mechanism by increasing the cellular abundance of ceramide, dihydroceramides, hexosylceramide, lactosylceramide, and sphingomyelin. Moreover, the study demonstrated that combining FASN and PARP inhibition has synergistic effects, significantly reducing cell proliferation and inducing cell death. Our findings suggest a promising strategy to enhance the effectiveness of existing CRPC therapies. Targeting FASN deprives cancer cells of their “fuel” and sensitizes them to the DNA-damaging effects of PARP inhibitors.