Importantly, we observed that NEO212 blocked autophagy flux which significantly facilitated it induced apoptosis and was largely because NEO212 inhibited the nuclear translocation of transcription factor EB (EB), and impaired the lysosomal function, implying NEO212 might avoid from autophagy mediated chemoresistance, thus proposing NEO212 as a potential therapeutic candidate for ovarian cancer. The gene discussed is TFEB; the disease is ovarian cancer.