Since HT29 cancer cells are wildtype regarding Kirsten rat sarcoma virus (K-Ras) mutation, it cannot be ruled out that this observed phenomenon is partly mediated by the RAS/extracellular-signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/Akt pathways, with a close connection to the pro-inflammatory factors like IL17, IL22, and IL23 [161]. This evidence concerns the gene AKT1 and cancer.