AKT1 and urinary bladder cancer: The other mechanism of acquired resistance, which involved ErbB2/3 activation in a rapid, reversible and ligand-dependent manner, was observed in a study of resistance to BGJ398 in the RT112 bladder cancer cell line.29 In this study, total and p-Met were undetectable in the BGJ398-resistant cells, in contrast to our findings of the exclusive activation of Met signaling mediating ErbB3-dependent or -independent activation of PI3K/AKT signaling seen in H1581AR and H1581BR cells.