In an effort to ascribe a presumable function to the gene-specific intron retention process herein identified, and given that approximately 50% of all human miRNAs reside within introns of coding genes [51], with certain intronic species (miR-211) critically modulating the malignant and invasive characteristics of melanoma [52], we assumed that the c-MYC, MCT4, and Sestrin-1 retained introns could serve as sources of miRNA generation. The gene discussed is SESN1; the disease is melanoma.