Several resistance mechanisms have been reported for CDK4/6 inhibitors and ET, such as the Cyclin E/CDK2 axis, mitogen-activated protein kinase (MAPK) pathway alterations, and tumor microenvironment alterations [36,37]; therefore, a precise understanding of the other resistance mechanisms would help predict preclinical models or populations to show the antitumor activity of tasurgratinib in combination with ET with high precision. This evidence concerns the gene CDK2 and neoplasm.