It has selectively constrained the growth of prostate tumor cells by inducing STAT3 dephosphorylation at Try705 and inhibited its localization to the nucleus, leading to the inhibition of expression of STAT3 target genes such as cell survival-related genes (cyclin D1 and survivin) and anti-apoptotic proteins (Bcl-2 and Bcl-xL) and thereby inhibiting the growth of STAT3-activated tumor cells. This evidence concerns the gene STAT3 and neoplasm.