To unravel the primary mechanism of action by which CBSI treatment impairs vincristine-resistant neuroblastoma cell viability, we examined intracellular alpha-tubulin by immunofluorescence in VCR-SK-N-AS and VCR-Kelly cells treated for 24 h with either 100 nM 4h and 500 nM 4k compared to a matched DMSO control. This evidence concerns the gene TUBA1B and neuroblastoma.