Similar to our findings when employing SKBR3 cells, autophagic activity was significantly elevated in Tzb-naive HER2-dependent BT474 breast carcinoma cells, whereas Tzb treatment failed to modulate autophagosome-related LC3 expression, lysosomal function and p62 expression in HER2-negative MCF-7 cells, Together, these data point to HER2 as required element in the cascade of events leading to autophagy following exposure to the anti-HER2 monoclonal antibody Tzb. The gene discussed is MAP1LC3A; the disease is breast carcinoma.