However, further analysis showed that the observed inhibition of prostate cancer growth by these compounds was mediated by PPARγ-independent mechanisms such as the inhibition of the CXCR4/CXCL12 axis, or the Bcl-xL/Bcl-2 functions or the suppression of the androgen receptor expression [14,15,16]. Here, PPARG is linked to prostate carcinoma.