Although inhibition of FANCF is known to result in FANCD2 ubiquitination inactivation and dysfunction of the FA/BRCA pathway, which enhance the sensitivity of cancer cells to DNA cross-linking agents, such as cisplatin, mitomycin and melphalan in ovarian, breast cancer, and myelomas [25–27], little is known about which gene depletion in the upstream core complex is of a stronger sensitizing effect to cisplatin in drug-resistance lung cancer cells. The gene discussed is FANCD2; the disease is breast cancer.