STAT3 and its associated factors (i.e., IL-6) have been shown to have a crucial role in pro-survival and growth of PCa cells in androgen-depleted condition.28, 29, 30 Our data clearly show that DAB2IP could inhibit STAT3 activity through dephosphorylation of its two residues, tyrosine 705 and serine 727, both of which are critical for STAT3 dimerization and transactivation,31, 32 and then selectively control the expression of these target genes (i.e., survivin and Bcl-2) in vitro and in vivo. The gene discussed is STAT3; the disease is posterior cortical atrophy.