For instance, in idiopathic pulmonary fibrosis, H3K18la facilitates the transcription of YTHDF1, promoting the expression of m6A‐modified NREP.[40] Similarly, H3K18la has been shown to activate the transcription of NSUN2 in colorectal cancer,[41] while increased H3K18la in neurons stimulates Piezo2 transcription.[42] We established that H3K18la contributes to HECTD2 transcription in HCC, ultimately restricting the response to lenvatinib treatment. Here, HECTD2 is linked to idiopathic pulmonary fibrosis.