Alternatively, mutations within the forkhead domain could affect FOXA1's affinity for its canonical binding site, potentially resulting in binding to new genomic locations, which may result in substantial effects on the transcriptional program within that tumor, for example FOXA1's recruitment to novel sites in the CRPC cell line LNCaP-abl, allows it to become androgen independent (Zhang et al., 2011). Here, FOXA1 is linked to neoplasm.