Apart from tendons, the upregulation of miR-29 has been shown to reduce muscular atrophy and renal fibrosis via the downregulation of α-SMA, fibronectin, and COL I. Moreover, deficiencies in certain variants of miR-29 have been linked to immunological conditions such as multiple sclerosis and various types of lymphomas [104,105]. Here, ACTA1 is linked to muscular atrophy.