Beyond the loss of LATS1/2 (key regulators of the Hippo signaling pathway) —which suppresses MHC-I transcription—endometrial tumors can also undergo LC3-mediated selective autophagic degradation of NLRC5, the master transcriptional activator of MHC-I genes, thereby further diminishing tumor visibility to cytotoxic T cells (53, 54). The gene discussed is LATS1; the disease is neoplasm.