NSD2 and lung adenocarcinoma: Importantly, previous studies have revealed that NSD2‐catalyzed H3K36me2 participates in crosstalk with other histone marks, such as excluding H3K27me3 in lung adenocarcinoma.[24] Consistently, we found that the level of H3K27me3 was significantly increased in Nsd2‐deficient mice (Figure S8A,B, Supporting Information), indicating that loss of NSD2 results in repression of gene expression.