SF-20, or MYDGF, is a Bone marrow-derived monocyte protein, and it is correlated with enhanced metabolic activity, suppression of apoptosis, and stimulation of cell proliferation. MYDGF is expressed predominantly in inflammatory cells, such as monocytes and macrophages. Up-regulation of MYDGF expression was also found during adipocyte differentiation. Expression of MYDGF was induced in the circulation and heart tissue after myocardial infarction. It promotes cardiac myocyte survival by stimulating endothelial cell proliferation through a MAPK1/3-, STAT3- and CCND1-mediated signaling pathway, and inhibits cardiac myocyte apoptosis in a PI3K/AKT-dependent signaling pathway. MYDGF was found over-expressed in approximately two-thirds of Hepatocellular Carcinoma (HCC) tissues, and its expression was significantly positively correlated with that of alpha-fetoprotein (AFP). In HCC, MYDGF could regulate cell proliferation through activating Akt/mitogen-activated protein kinase pathways. Mouse MYDGF shares 92% amino acid sequence identity with both human and rat MYDGF. Intriguingly, virtually all homologs of MYDGF have a C-terminal putative ER retention sequence BXEL (B: Arg, His, or Lys; X: variable residue; E: Glu; L: Leu), which has the potential to retain human MYDGF and its homologs in the ER, whereas truncated MYDGF without BXEL is secreted from the cell. However, the functions of these different forms remain unclear.