These sexually dimorphic differences in dimer formation have been attributed to STAT5A having a longer refractory period to reactivation by GH than STAT5B [32, 33], but we show that these differences may be due to GH signalling in the skeletal muscle being predominately inhibited by SOCS2 in female mice and by CIS in male mice. Here, STAT5A is linked to in situ carcinoma.