A model of how HTLV-I can up-regulate telomerase gene expression and function in the absence of the viral tax oncoprotein. Upon IL-2 stimulation, PI3K transcriptionally up-regulates telomerase (hTERT) gene expression, whereas Akt increases telomerase function by phosphorylating hTERT protein. LY29 and AKTII, known pharmacological inhibitors of PI3K and Akt, respectively, reduce telomerase activity, confirming the involvement of the PI3K/Akt pathway in activating telomerase function. IL2 stimulation also results in sequestration of WT1, a known transcriptional repressor of hTERT gene, in the cytoplasm of the cell, thereby increasing telomerase gene expression and function.