Returning to the example of spinal muscular atrophy, the complementing SMN2 paralog contains in its 5’ region a number of STAT5 kinase binding sites; it has been recently shown that the STAT5 activating hormone prolactin both upregulates SMN protein derived from SMN2 and confers significant survival benefit in a mouse model of SMA [31]. This evidence concerns the gene PRL and proximal spinal muscular atrophy.