Phosphorylation of serine 68 of ELF3 was demonstrated to participate in nuclear import, accumulation and retention of ELF3 in Kras mutated lung adenocarcinoma [17] The partial competition between S68A ELF3 mutant and KLF10, especially in Notch-3 gene promoter activity, may be attributed to multiple binding sites of ELF3 on Notch-3 promoter with various affinity and inherent levels of KLF10/ELF3 in Panc-1 cells. This evidence concerns the gene KRAS and lung adenocarcinoma.