Concomitant treatment led to an increase in apoptosis, cell-cycle arrest, and modulated the protein expression of the JAK/STAT3, MAPK (ERK, p38), PI3K/Akt, and NF-κB involved in the progression and development of colorectal cancer (Riahi-Chebbi et al., 2019). This evidence concerns the gene AKT1 and colorectal cancer.