Additionally, the expression levels of RFC3 and RFC5, which bind RFC4 to form a core polymerase accessory complex, were rarely upregulated in NSCLC tissue compared to adjacent normal lung tissue (Supplementary Fig. 5a), and silencing RFC2 or RFC5 or silencing the essential DNA replication accessory gene PCNA reversed the promoting effects of RFC4 on NSCLC cell proliferation but failed to interfere with RFC4-induced Notch1 signaling activation or RFC4-potentiated tumor invasion and stemness in vitro or tumor metastasis and tumorigenicity in vivo (Supplementary Fig. 5b–i). This evidence concerns the gene RFC5 and neoplasm.