A recent study by Ooki, et al., (2018) demonstrated that in bulk lung cancer populations the promotor of the transcription factor PAX6 was methylated, resulting in its repression, while in CSCs PAX6 was not methylated and promoted transcription of the hedgehog regulator GLI, resulting in an upregulation of SOX2, OCT4, and NANOG, driving cancer cells toward a stem-like state 78. This evidence concerns the gene PAX6 and lung carcinoma.