DCLK1 and lung cancer: In certain colorectal, pancreatic, gastric, and lung cancers, this 5′α-promoter has been shown to be hypermethylated, resulting in epigenetic silencing [55,56,57,58,59] and transcriptional upregulation of the two alternative short isoforms (DCLK1-BL (isoform 4, 433 aa), DCLK1-BS (isoform 3, 422 aa)) via the alternative 3′β-promoter in intron V, which is activated by the transcription factor NF-κB [58].