In liver cancer, linc‐UFC1 promoted proliferation and reduced apoptosis in HCC cells through directly interacting with the mRNA‐stabilizing protein HuR to regulate levels of β‐catenin.12 In colorectal cancer, linc‐UFC1 silence induced cell proliferation inhibition and G1 cell cycle arrest via suppressing β‐catenin and activating phosphorylated P38.13 Recent studies reported that many RNA transcripts, such as lncRNA, function as competing endogenous RNAs (ceRNAs) by competitively binding common microRNAs.15, 16 However, to date, whether linc‐UFC1 functions as a ceRNA remains unknown. The gene discussed is ELAVL1; the disease is colorectal cancer.