Furthermore, RNase1 as an anti-inflammatory mediator cleaves excess exRNAs to prevent exRNAs-induced elevation of proinflammatory cytokines, such as tumor necrosis factor-α, in cardiovascular pathophysiology and in a xenograft mouse model of colon carcinoma HT-29 cells, leading to cardiomyocyte function protection and tumor regression, respectively 21-23. This evidence concerns the gene RNASE1 and neoplasm.