High-throughput CRISPR screens have demonstrated possible mechanisms of nongenetic resistance, including loss of PRC1.1 subunits and therefore derepression of noncanonical Menin targets, including MYC, and a failure of molecular switching to UTX-KMT2C/D transcriptional regulation of tumor-suppressive programs upon Menin inhibition [94,95]. Here, MYC is linked to neoplasm.