Overexpressing HULC could enhance cancer cell proliferation, migration and invasion.[24, 25, 18] Preliminary research in the mechanism of HULC found that it could co-purify with ribosomes in the cytoplasm and play a role in post-transcriptional modulation of gene expression.[26, 27] Research has identified that HULC could perturb the circadian rhythm of cancer cells and contribute to the epithelial-to-mesenchymal transition (EMT), required for cancer metastasis and invasion.[19, 27, 25, 24] In addition, HULC knockdown could enhance cisplatin-induced apoptosis in cancer cells. The gene discussed is HULC; the disease is cancer.