CDK6 plays a pivotal role in cell cycle progression.[19] FAT1 loss induces CDK6 expression through the Hippo pathway and plays an important role in CDK6 amplification, and this is the hallmark of CDK4/6i resistance.[26] In a clinical study, targeted sequencing was performed on 348 tumor samples obtained before patients were treated with CDK4/6i, and the results showed that loss of functional mutations in the FAT1 tumor suppressor gene leads to resistance to CDK4/6i, and FAT1 upregulates CDK6 expression through the HIPPO pathway.[27]. Here, CDK4 is linked to neoplasm.