AKT1 and neoplasm: Xu et al were the first to illustrate the relationship between snoRNA and HCC, which indicated that snoRNA SNORD113-1 in HCC could inactivate the intracellular phosphorylation of ERK1/2 and SMAD2/3, demonstrating its tumor-suppressing function.[19] In contrast, SNORD126 overexpression in HCC was shown to function as a tumor-promoting snoRNA by increasing fibroblast growth factor receptor 2 expression and activating the PI3K-AKT pathway.[20] Moreover, according to a recent study by McMahon et al, HCC patients with low SNORA24 expression tend to exhibit poor long-term survival.[21]