The transcription factors STAT5a and STAT5b are being constitutively activated in multiple human tumor types.[1] Despite their high degree of sequence homology (96 % on the protein level), they have both redundant and non‐redundant functions.[2] While STAT5b has been identified as the main driver of cell growth and tumorigenesis,[2e, 2f, 2g, 2h, 2i, 2j] the ability of STAT5a to compensate for STAT5b in many functions makes a supporting role for STAT5a during tumorigenesis likely. This evidence concerns the gene STAT5B and neoplasm.