Complementary to these results, Ding and co-workers have shown that the expression levels of the SESN1 and/or SESN2 genes are often diminished in human lung cancers and suppression of SESN1/2 may support tumour growth and/or progression through such mechanisms as stimulation of cell growth, proliferation, mutagenesis and angiogenesis. The gene discussed is SESN1; the disease is neoplasm.