Several lines of evidence support this supposition: 1) Exogenous MSU rapidly activated the MAP kinase pathway (Figure 7A); The inhibition of the MAP kinase pathway blocked MSU-induced MICA/B expression; 2) Inhibition of uric acid production by allopurinol in tumor cells undergoing genotoxic stress inhibited MAP kinase activation (Figure 10) and MICA/B expression (Figure 3); 3) We and others showed that RAS and BRAF oncogene mutation and activation leads to increased MICA/B expression [12, 14]; 4) The promoters of both the MICA and MICB genes contain a putative AP-1 site [18]. This evidence concerns the gene MICB and neoplasm.