As far as MCL cells are concerned, however, it remains to be elucidated whether the aberrant expression of TLR2 and TLR5 is a consequence of malignant transformation or just a reflection of the phenotype of the putative MCL cell precursor, as already described for other types of B-cell malignancies.[34] Furthermore, shortage of growth factors within tumor microenvironment may lead to up-regulation of TLR2 and, to a lesser extent, of TLR5, as shown by culture of MCL cells under low serum conditions. The gene discussed is TLR2; the disease is neoplasm.