VIM and neoplasm: We hypothesize a possible molecular mechanism of miR-CT3, which might (1) control tumor angiogenesis by direct link with VEGF-A, passing also through the inactivation of the MAPK/ERK pathway, and (2) counteract the migration and invasion of OS cells, through the inhibition of some EMT proteins, such as Vimentin, passing through the activation of p38 MAPK pathway (Figure 8).