Furthermore, the combined knockdown of key autophagic factors ATG7 and ATG3 in HeLa cells and ovarian cancer cells (OVCAR8) led not only to TWK-independent inhibition of autophagic flux (assayed by LC3 lipidation) as expected, but also to accumulation of endogenous Fn14 (Fig. 2c and Supplementary Fig. 2d) without affecting EGFR levels (Supplementary Fig. 2e). The gene discussed is EGFR; the disease is ovarian carcinoma.