The GATA3 mutations (n = 15) all reside in intron four of the gene and most are INDELs from breast cancer (n = 11) that disrupt the acceptor splice site, which leads to abnormal splicing and codon frame shift as described previously for the luminal-A subtype of breast cancer.10,11 In addition, one lung adenoma SNV also disrupt the splice site. This evidence concerns the gene GATA3 and lung adenoma.