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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)

By inhibiting NNMT, it leads to an increase in intracellular levels of NAD+ (nicotinamide adenine dinucleotide), a critical coenzyme for cellular metabolism and mitochondrial energy production

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The ANDROMEDA study has shown that daratumumab, a monoclonal antibody targeting human CD38, may improve patient prognosis in AL amyloidosis [96]