Several preclinical studies have proven the efficacy of MBZ as an inhibitor against multiple processes that are accountable for tumor resistance and progression at nano- and micro-molar clinically reachable concentrations, including dysregulated angiogenesis, protein kinase activation and expression (including BCR–ABL, BRAF, VEGFR2 and MEK), matrix metalloproteinase 2 and multi-drug resistance protein transporters MRP1 and p-gp and pro-survival pathways (such as c-MYB, XIAP, SHH and MAPK/ERK) [9]. This evidence concerns the gene SHH and neoplasm.