In line with this, we found that increased pRPA levels and decreased replication fork speed induced by SIRT5 knockdown were recovered by nucleoside supplementation (Fig. 2h and Supplementary Fig. 2f), suggesting that nucleotide deficiency is accountable for replication stress-induced DNA damage in SIRT5-knockdown CRC cells. The gene discussed is SIRT5; the disease is colorectal carcinoma.