In 2021, Bertozzi’s group reported GalNAc-LYTACs to degrade target such as EGFR and HER2.378 Their GalNAc-LYTACs effectively ablated EGFR and HER2 in HCC cells depending on the lysosomal system and the internalization of ASGPR.378 Moreover, in 2024, Xu et al. designed EGFR-ATTECs also using the LC3 ligand GW5074 to degrade EGFR, the result indicated that the ATTECs could induce EGFR degradation and exerted anti-proliferative effects with moderated safety.379 These technologies employ distinct mechanisms to target and dismantle EGFR, potentially offering new therapeutic avenues in oncology. This evidence concerns the gene EGFR and hepatocellular carcinoma.