UVRAG and cancer: Moreover, UVRAG prevented accumulation of abnormal chromosomes, although it is not clear whether this feature is autophagy dependent.74 Bif‐1 interacts with Beclin‐1 and UVRAG and also serves to activate autophagy.44 Consequently, loss of Bif‐1 expression reduces autophagy and in knockout mice resulted in an increased number of spontaneous tumors.44 Together with the above‐described data on Beclin‐1, these findings suggest that autophagy regulation by Beclin‐1 is an important hub that is deregulated in cancer.