To glean more insights into reprogramming of EV communication mechanisms in cancer, we modelled RAS‐driven EV uptake in a series of isogenic cell lines including non‐transformed epithelial cells of intestinal (IEC18) or mammary origin (MCF10A) and their corresponding aggressive variants harbouring mutant HRAS (V12; RAS3 and MCF10AT, respectively) (Figure 1a, Fig. S2). The gene discussed is HRAS; the disease is cancer.