AKT1 and colorectal cancer: By attenuating the negative feedback regulation mediated by downstream p70S6K under growth factor stimulation, this protein upregulates AKT phosphorylation levels, thereby enhancing AKT activity, promoting epithelial‐mesenchymal transition (EMT), and significantly reducing the sensitivity of colorectal cancer cells to therapeutic drugs.[81] iii) Drugs interfering with each other's biotransformation processes, resulting in significantly weakened efficacy or adverse reactions.