Bladder cancer is associated with various polymorphisms in the human genome, many of which are localized in intergenic, regulatory and intronic regions where genes for non-coding RNA and mobile elements are located. Therefore, the discovered associations exert their influence on bladder cancer development by changing the activity of non-coding RNAs and mobile elements. This is reflected in DNA methylation abnormalities, since miRNAs serve as guides for RNA-dependent DNA methylation and retroelements are competing endogenous RNAs for miRNAs. Scientific literature analysis has shown the involvement of a large number of long non-coding RNAs and microRNAs in bladder cancer development. These molecules can function as oncogenes and as tumor suppressors depending on their target genes. A combined effect of long non-coding RNAs with microRNAs (TINCR/miR7, RP11-89/miR-129-5p, CASC11/miR-150, LUCAT1/miR-181c-5p, KCNQ1OT1/miR-218-5p, GAS6-AS6/miR-298, BCCE4/miR-328-3p, KCNMB2-AS1/miR-374a, SNHG1/miR-493, TUG1/miR-582-5p, UCA1/miR-582-5p, LINC00958/miR-625, DDX11-AS1/miR-2355-5p, ARAP1-AS1/miR-3918, BACH1-IT2/miR-4786) was revealed, as well as the role of 28 retroelement-derived microRNAs in bladder cancer carcinogenesis. The activation of retroelements, which serve as drivers of epigenetic regulation, has been described and confirmed in a number of clinical studies.