IHC analyses showed that the expression of USP5 in the residual tumors derived from the KrasG12D-shUSP5 was similar to the tumors derived from the control KrasG12D mice in the absence of shUSP5 (Supplementary Fig. S6c), suggesting that the presence of USP5 expression is most likely responsible for the residual tumor growth. This evidence concerns the gene USP5 and neoplasm.