Thephosphorylation of RXRαabolishes its ability to form heterodimers with RARβ,thus resulting in the loss of cell growth control, resistance to retinoids, andthe acceleration of cancer development [27].These findings suggest that the accumulation of p-RXRα(i.e., nonfunctional RXRα),which can escape from the proteasome-mediated degradation system, may interferewith the function of normal RXRαin a dominant-negative manner, thereby playing a critical role in thedevelopment of HCC (see Figure 2) [28]. This evidence concerns the gene RARB and cancer.