Activation of the Wnt/βcatenin pathway combined with oxidative stress metabolism and RAS/ERK pathway, loss of tumour suppressor genes, and mutations in chromatin regulators are most frequently observed; overexpression or activation of receptor tyrosine kinases such as ERB2 and MET, of the mTOR pathway, as well as CMYC (ref. 2) and the transcriptional co-activator YAP1 (ref. 3), are observed with varying frequency. This evidence concerns the gene YAP1 and neoplasm.