MAPK3 and neoplasm: 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.