In addition, compared to the cells of individual TAX treatment, the co-treatment of TAX and Recilisib (an agonist of PI3K/AKT signaling) increased the proliferation and colony formation of androgen-independent PCa cells, and up-regulated the expression of c-Myc, cyclin D1, p-AKT and FGFR2 (Fig. 3), which means that the re-activation of PI3K/AKT could partially abolish the anti-proliferation effect of TAX on androgen-independent PCa cells. The gene discussed is FGFR2; the disease is posterior cortical atrophy.