Moreover, to clarify the role of mTORC1 signalling in Kdm6a-dependent tumour suppression, we used hydrodynamic delivery of a transposon vector expressing c-myc in conjunction with double CRISPR/Cas9 constructs targeting Kdm6a and Mtor or S6K1, two key downstream molecules of mTORC1 signalling, simultaneously. This evidence concerns the gene MYC and neoplasm.