With respect to the mechanisms, our study identified CAPZA1 as a novel substrate of UBR5 and suggested that UBR5 mediated the ubiquitin-proteasome-dependent degradation of CAPZA1, which in turn facilitated pancreatic cancer metastasis via promoting F-actin remodeling (Figure 6). The gene discussed is CAPZA1; the disease is familial pancreatic carcinoma.