The results revealed that CRC cell-derived EVs with MIR181A1HG overexpression or silencing apparently promoted or inhibited the phosphorylation of Smad2/3 in LX2 cells, respectively, whereas the overexpression or knockdown of miR373-3p partially neutralized these effects, respectively (Fig. 4q). The gene discussed is SMAD2; the disease is colorectal carcinoma.