Tumor resistance to PTX involves several mechanisms, including efflux pump modification, epithelial–mesenchymal transition (EMT), kinase-dependent cyclin 1 (CDK1), the cell death signaling pathway, and finally, the overexpression of a less PTX-sensitive β-tubulin isotype β-III, which has been consistently reported in many types of acquired PTX-resistant cancers [10,11,12,13]. This evidence concerns the gene CDK1 and neoplasm.