These approaches generally do not address (i) the influence of STAT1 on the tumour microenvironment, (ii) the interaction of STAT1 expressing HNSCC cells with immune cells, stromal cells, and fibroblasts and (iii) the impact of STAT1 activation by oral epithelial cells on HNSCC tumour initiation and promotion. This evidence concerns the gene STAT1 and neoplasm.