The CAAI borussertib, despite being more efficacious compared with other AKT inhibitors, and despite showing anti-proliferative effects in cancer cell lines harboring alterations of the PI3K/AKT pathway, as well as in a KRAS-mutant xenograft model in combination with a MEK inhibitor, has a poor pharmacokinetic profile, making it difficult to achieve an effective therapeutic dose with oral application [302, 325]. The gene discussed is PIK3CA; the disease is cancer.