For example, SF3A3 was shown to synergize with YTHDF2 to drive hepatocellular carcinoma progression,[32] and to selectively regulate MYC‐driven splicing and metabolic reprogramming in breast cancer, where SF3A3 levels modulate MYC‐induced plasticity and oncogenesis.[21] In non‐small cell lung cancer, circSCAP can interact with SF3A3 to suppress malignancy, and in bladder cancer, E2F6/KDM5C promotes SF3A3 expression through a hypomethylated promoter region.[19, 20] More recently, structural studies by Shi et al. This evidence concerns the gene KDM5C and urinary bladder cancer.