Some of these interactions involve the upregulation of CD38, mediated by adipocyte-secreted angiotensin II (Ang II), which has been identified as the direct cause of increased expression of acetyl-CoA synthetase (ACSS2) in MM plasma cells, promoting growth by stabilizing the oncoprotein IRF4 in vitro and in vivo (95). Here, ACSS2 is linked to Miyoshi myopathy.