In order to assess whether these identified candidates indeed drive the elevated YAP/TAZ activity phenotype, we performed siRNA-mediated knockdown of RELN or RBCK1 in HS578T breast cancer cells, followed by expression quantification of YAP/TAZ canonical targets, which serves as a read-out of nuclear YAP/TAZ activity (Piccolo et al., 2014). This evidence concerns the gene WWTR1 and breast carcinoma.