Yao X et al. found that reintroduction of Bit1 was sufficient to suppress the anchorage-independent growth; conversely, Bit1 downregulation significantly enhances anchorage-independent growth in A549 cells and further investigation revealed that the Bit1-depletion cells displayed significantly enhanced tumorigenecity in vivo [18], implying Bit1 functions as tumor suppressor in lung carcinoma. The gene discussed is PTRH2; the disease is neoplasm.