This was brought about by possibly promoting cell proliferation, as observed by in vitro and in vivo experiments.146 Further, MALAT1 has been reported to be secreted by CRC tumor cells to mediate disease progression using their competing endogenous RNA (ceRNA) function by sequestering miR-26a/26b and regulating Fucosyltransferase 4 (FUT4) fucosylation to activate the PI3K/AKT pathway.147 While this study specifically proposes a role mediated by EV-derived MALAT-1, the validation on patient samples is indirect and only associative. The gene discussed is FUT4; the disease is colorectal carcinoma.