Given that RPL26 is identified as an ufmylation target by UFM1-captured proteomics analysis [15, 16], it would be interesting to see if RPL10 ufmylation really occurs in pancreatic cancer cells, what enzyme system would be responsible for this modification, whether RPL10 ufmylation is associated with cell stemness and whether interference of RPL10 ufmylation would exhibit antitumor activity. This evidence concerns the gene RPL26 and familial pancreatic carcinoma.