Moreover, MA treatment downregulated the expression of the Akt1 gene, which codes for the protein AKT (protein kinase B, PKB) (Figure 3), a serine/threonine kinase critical in controlling cell survival, insulin signaling, angiogenesis, and tumor formation; the Tpr53 gene (Figure 3), encoding protein p53, which regulates cell cycle, apoptosis, senescence, metabolism, and DNA repair; the Msh6 gene (Figure 3), involved in the post-replicative DNA mismatch repair system (MMR) and the Tgfb1 gene and its receptor (Tgfb1r1) (Figure 3). This evidence concerns the gene INS and neoplasm.