By contrast, MCC-L1-α, the homozygous L1 insertion in donor 95, severely reduced MCC transcription in both tumor (−83%) and nontumor (−63%) samples compared with normal liver controls (Figure 4B), demonstrating that the primary effect of MCC-L1-α was on MCC rather than APC. These data in sum confirmed that (1) L1-mediated retrotransposition in MCC specifically repressed MCC and not APC and (2) CTNNB1 was strongly induced in all four affected individuals, indicating activation of a major HCC oncogenic pathway. Here, CTNNB1 is linked to neoplasm.