TAT 212) was held in Amsterdam, the capital of the Netherlands. TAT212 is an official cooperation meeting of the European Society of Oncology (ESMO), sponsored by the NDDO Education Foundation in Amsterdam and co-organized by the National Cancer Institute (NCI). Phosphatidylinositol -3- kinase (PI3K) pathway is often found to be activated in tumor patients, which plays an important role in tumor progression and resistance to tumor drugs (including cytotoxic chemotherapy drugs and targeted drugs). There are several kinds of molecular aberrations that affect the key components of this pathway, including gene mutation and amplification (PIK3CA, AKT) and negative regulatory factor dysfunction (PTEN). PI3K pathway inhibitors are still in the early stage of clinical research and development, including: (a) simple pan-PI3K inhibitors; (b) Dual-target PI3K/mTOR inhibitors; (c)AKT inhibitors; (d) inhibitors of d)mTOR complexes 1 and 2; (e)PI3K subtype specific inhibitors. Studies have found that these inhibitors can partially relieve tumors and prolong the stable period of the disease in many types of tumors (breast cancer, gynecological tumor, prostate cancer, lung cancer, mesothelioma, sarcoma and lymphoma), but the effect is not as good as expected. Pharmacokinetic (PD) studies show that reducing the activation level of key pathways in tumors and related tissues can significantly reduce the level of proliferation markers and the uptake value displayed by FDG-PET, thus proving that the target has been hit. Related clinical benefits are not limited to tumor patients with PI3K pathway activation, and PD markers have not been found to have clear predictive value. It should be emphasized that based on preclinical studies, the anti-tumor activity of PI3K pathway inhibitors against oncogene-controlled malignant tumors (such as PIK3CA and PTEN mutations) is still unclear. However, it is clear that inhibiting PI3K pathway can lead to compensatory receptor tyrosine kinase excitation and adaptive negative feedback, thus proving the adaptability of oncogene network. Therefore, the future research on PI3K pathway inhibitors should focus on the combination therapy strategy, including the combination of targeted agents such as BRAF, MEK, EGFR and HER2 inhibitors. It is very important to understand the role of PI3K pathway inhibitors in the study of combined drugs. If the results show that PI3K pathway inhibitors lack clinical activity, but the reason is that the pathway has not been effectively inhibited, researchers should improve the dosage and regimen, provided that the toxic reaction can be tolerated. On the contrary, if it is for other reasons, we should make great efforts in tumor biology research. These studies are worth looking forward to.