Accordingly, knocking out NUAK2 with CRISPR, blocking expression with RNA interference (RNAi) or pharmacological inhibition of NUAK2 activity drives cytoplasmic localization of YAP/TAZ, inhibits YAP/TAZ transcriptional activity, attenuates the growth of diverse cancer cell lines in culture, and decreases tumor growth in an orthotopic breast cancer mouse model. This evidence concerns the gene YAP1 and neoplasm.