Instead, evidence accumulated thatalternative (“nongenomic”) PPARγ signaling pathways, crosstalk with the ERK cascade and elevated PPARγ expression levels in certain tumortypes (where PPARγ is postulated to act as a prosurvival factor, e.g., in hepatocellularcarcinoma, squamous cell carcinoma), are the cause for the observed tumorpromoting effects of PPARγ ligands, and may explain the absence of clear therapeutical benefit ofTZDs in cancer patients [78, 79, 143]. This evidence concerns the gene PPARG and squamous cell carcinoma.