For example it was shown that cancer cells overexpressing pp32r1 or a pp32r1Y140H functional mutant in the ANP32C oncogene that is overexpressed in breast, prostate and pancreatic tumours, may demonstrate enhanced resistance to FTY720 treatment through conserved residue F136, likely to be a key determinant of the FTY720 binding site [247]. The gene discussed is ANP32CP; the disease is cancer.