Thus, the enhanced expression of S100B in melanoma cells has been suggested to be causally related to tumor progression given that S100B not only interacts with the tumor suppressor, p53, blocking its phosphorylation [18] but also downregulates p53 expression (with p53 in turn downregulating S100B expression) [19], and pharmacological blockade of S100B activity with pentamidine, a drug that disrupts S100B-p53 interactions [20], results in a significant tumor growth inhibition [21]. The gene discussed is S100B; the disease is neoplasm.