It is suggested that the antiangiogenicactivity of PPARγ can be accomplished either by blocking the production the angiogenicELR+CXC chemokines by cancer transformed cells or by inducing expression of thethrombospondin-1 receptor CD36 in endothelial cells [42–44] Inaddition, latest exciting data, which showed that PPARγ agonists were able to inhibit thecanonical WNT signaling in human colonic epithelium, raises hopes that suchagents can possibly block cancer initiation at a stem cell level [45]. Here, CD36 is linked to cancer.