Theantitumor effect of RNase A that we observed can occur due to (1) the degradation of encodingintracellular RNAs and, as a consequence, (a) the arrest of protein synthesis [26, 27] and (b) thealteration of gene expression profile via RNA cleavage products [28]; (2) the degradation of noncoding RNAs (pre–miRNAs, miRNAs, andsiRNAs) [2, 29];(3) the destabilization of the RNA structure [30]; (4)the blockage of RNA functions [31]; (5) the influence onsignaling pathways [32–34]; and (6) the cutoff of uncontrolled potassium influx viacalcium–dependent potassium channels of tumor cells [35]. This evidence concerns the gene RNASE1 and neoplasm.