Besides poor bioavailability due to inefficient recovery from the precursor, it was later discovered that the 10-hydroxy substituent introduced into the structure of SN38 increased its affinity toward ABCG2 [11,22], likely contributing to the unremarkable results observed with irinotecan in preclinical models of immature neuroblastoma with MYCN amplification [23,24] and to a lack of efficacy when tested in children with aggressive disease [25]. The gene discussed is ABCG2; the disease is neuroblastoma.