While the long and ΔS1 PRLr isoforms, originally isolated from T47D breast cancer cells, may activate proliferative signalling through the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, the short isoforms IF, S1a and S1b lack the tyrosine rich residue required for full STAT binding [20], [21], [22], [23]. The gene discussed is PRLR; the disease is breast carcinoma.