Taken together, these data indicate that both p53 null and mutant p53-expressing tumour cells release exosomes in similar quantities, but those from mutant p53-expressing cells upregulate RCP and DGKα-dependent receptor recycling in p53 null recipient cells to evoke migratory characteristics associated with mutant p53’s invasive gain-of-function. The gene discussed is DGKA; the disease is neoplasm.