First, overexpressing p23 (p24δ1) or a p25 (p24α2) mutant protein in cultured mammalian tumor cells resulted in the formation of Golgi mini-stacks and highly specialized lipid subdomains, respectively, leading the investigators to conclude that p24 proteins are involved in the formation of membrane subdomains in the early secretory pathway [13], [14]. Here, TMED2 is linked to neoplasm.