During tumor development, several oncogenes and tumor promoters are translationally controlled by hnRNPA1, including FGF-2, c-MYC, CCND1, XIAP, BCL-XL [52, 54, 55], etc. Nadiminty et al. [40] found that silencing hnRNPA1 and consequently of AR-v7 re-sensitizes cells to Enz treatment, indicating that upregulation of hnRNPA1 may confer resistance to anti-androgen therapies by promoting expression of the AR variants. Here, AR is linked to neoplasm.