SP1 and cancer: The data show that: (i) ACR suppresses the hyper-phosphorylation of RXRα, restored its transcriptional function, and enhanced the expression of TG2 and its nuclear accumulation, along with caspase 3 activation; (ii) Sp1 is crosslinked by TG2 and degraded by caspase 3, resulting in loss of its activity; and (iii) expression of Sp1-regulated target genes, such as EGFR (critical for cell survival), decrease, culminating in apoptosis of the cancer cells (Figure 5).