Therefore, the mechanism of action with which the poison of R. junceus could act against neoplasms could be through three mechanisms: a mitochondrial apoptotic action through the intrinsic pathway with an increase in the expression of p53 and an increase in the bax-BCL-2 ratio; the blocking action of the Na K and Cl canal, which would act on the concentration of intracellular calcium with a reduction in the capacity of variation of the shape and volume and, therefore, of tissue invasion; an influence on the CD 31- and Ki-67-mediated neoangiogenesis processes [20]. This evidence concerns the gene TP53 and neoplasm.