We next sought to investigate the downstream effects of BMP-SMAD4 activation in skeletal muscle of SBMA patients, and found no change in expression of BMP-negatively regulated FBXO30 [72], as well as other E3 ubiquitin ligases commonly upregulated in muscle atrophy (FBXO21, TRIM63) [7, 51], the master controller of muscle homeostasis HDAC4 [47] or other atrophy-related genes (FBXO32, ASB2), whose induction or repression directly depends on the TGFβ pathway [17, 72, 86], as previously observed [56, 67] (Supplementary Fig. 2, online resource). This evidence concerns the gene FBXO32 and Kennedy disease.