MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA‐23a (miR‐23a) negatively regulates the expression of two atrophy‐related E3 ubiquitin ligases, atrogin‐1 and MuRF1, in skeletal muscle and cultured muscle cells. During atrophy miR‐23a is reduced in muscle cells. Although it was recently shown that miR‐23a expression is positively regulated by NFATc3, the mechanism of miR‐23a suppression during atrophy remains unknown. Previously, we found that the activity of calcineurin (Cn), a calcium‐activated phosphatase that regulates NFATc proteins, is decreased by diabetes. Since diabetes causes muscle atrophy, and glucocorticoids are required for this response, we investigated how the glucocorticoid dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR‐23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h of treatment, Cn activity was reduced and less NFATc3 was present in the nucleus. Further, the level of miR‐23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR‐23a were decreased. Expression of atrogin‐1 and MuRF1 were also increased 48 h after DEX addition. Collectively, these findings indicate the Cn‐NFAT signaling pathway may play an important role in the regulation of atrogin‐1 and MuRF1 by suppressing miR23a during glucocorticoid induced muscle atrophy.Supported by the National Institutes of Health awarded to M.B. Hudson (T32 DK007656) and the American Heart Association to S.R. Price (7660020)