The inhibition of Hh signaling with cyclopamine or GANT-58 or the knockdown of TWIST1 and SNAI1 transcription factors attenuated the tumor-initiating cell properties of these multidrug-resistant sublines, as shown by reduced clonogenic, self-renewal, and sphere-formation ability, and restored their chemosensitivity to doxorubicin and vincristine. The gene discussed is SNAI1; the disease is neoplasm.