It suggests that activity of 17-aminogeldanamycin is at least partially independent of NQO1 that can be advantageous because a loss of NQO1 expression and acquisition of an inactive NQO1P187S variant have been demonstrated as causative factors in development of resistance to tanespimycin in melanoma and glioblastoma cells [69]. The gene discussed is NQO1; the disease is glioblastoma.