Even though numerous PPARγ-dependent mechanismshave been identified (for review see Tatenhorst et al., this issue), these datasuggest that PPARγ activation is not an imperative prerequisite for the inhibition of glioma cell viability in vitro, which is in line withprevious studies using human PC-3 and LNCaP prostate cancer and human A549 lungcarcinoma cells [11, 31]. The gene discussed is PPARG; the disease is prostate carcinoma.