Given that complete inactivation of Acsl4 in mice is compatible with life (61), and that targeting ACSL4 has the advantage of blocking the utilization of fatty acids in cancer cells regardless of whether they are synthesized de novo or acquired exogenously (62), it is tempting to speculate that pharmacological inhibition of ACSL4 may represent a particularly appealing and effective approach to treating RB1 loss–driven prostate cancer. The gene discussed is ACSL4; the disease is cancer.