Other than that, Liu et al. characterized PTX3 as the direct target of NAT10 through ac4C-seq and RNA-seq in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs); the mutant of PTX3 engineered to replace the ac4C consensus sequence CXX with GXX proved that the modification of ac4C mediated by NAT10 directly regulated PTX3 expression [48]. The gene discussed is PTX3; the disease is rheumatoid arthritis.