Activation of PPARγ by TZDs, by inducing apoptosis, growth arrest and cell differentiation in cancer cells, has been proposed as an explanation for the anticancer activity of these compounds (Blanquicett, Roman & Hart, 2008), together with PPARγ-independent mechanisms involving the proteosomal degradation of cyclins D1 and D3 (Lu et al., 2005), as well as the upregulation of PTEN/AMPK and the downregulation of the Akt/mTOR signaling pathways (Han & Roman, 2006). The gene discussed is PTEN; the disease is cancer.