Based on these findings, we proposed a model where drug resistance could synergize on CD15/FUT4 through at least two independent pathways: a) mitogenic intracellular due to ERBB2/ERBB3 overexpression; b) pro-angiogenic and/or mitogenic due to FGFR4 or IL-1β released by an altered tumor microenvironment as suggested by other studies (Fig. 4d) [35–37]. Here, ERBB2 is linked to neoplasm.