ENO1 and colorectal carcinoma: To further validate whether the oncogenic function of NSUN2 in regulating ENO1 depends on m5C methyltransferase activity, two enzymatically non‐functional mutants of NSUN2 were created by introducing point mutations at the release site (cysteine 271) or the catalytic site (cysteine 321), with the aim of disrupting its m5C enzymatic activity.[35] Indeed, overexpression of the wild‐type (WT) of NSUN2, but not mutant NSUN2 (NSUN2C271A or NSUN2C321A), led to the restoration of ENO1 mRNA (Figure 3L) and protein levels (Figure 3M) in NSUN2KO CRC cells.