Furthermore, the known cancer/testis antigen Plac1 was reported to interact with Furin, a proprotein processing enzyme92, to degrade Notch1 into Notch1 intracellular domain (NICD) fragments that undergo nuclear translocation to suppress PTEN transcription93, forming a Plac1/Furin/Notch1/NICD/PTEN signalling mechanism that results in transcriptional repression of PTEN and allows for the hyperactivation of AKT signalling in breast cancer (BC) cells93. The gene discussed is PLAC1; the disease is breast cancer.