These factors include alterations in molecules associated with gemcitabine transport and metabolism, such as the nucleoside transporter-1 (hENT1) [5], activation of tyrosine kinase genes such as c-Src [6], and aberrant expression of cellular survival genes, such as those involved in the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway [7] and alterations associated with the tumor microenvironment, among others [8,9]. The gene discussed is AKT1; the disease is neoplasm.