A key finding is that TLR2, with or without inhibitory AR activation, can directly stimulate proliferation of TLR2-high malignant oral squamous cells via the pro-oncogenic MAPK ERK1/2 pathway, as well as promote survival of these cells, thus potentially allowing some level of tumor cell autonomy from inflammatory cells in the context of microbial colonization and inflammation. This evidence concerns the gene AR and neoplasm.