PIK3R1 mutations that cause immunodeficiency through PI3-kinase hyperactivation also cause SHORT syndrome, due to PI3-kinase hypofunction, attributable to PI3-kinase destabilisation and outcompetition by mutant PIK3R1.

Beyond its well-accepted function in metastasis, non-receptor tyrosine kinase FER also controls ovarian tumor cell proliferation through FER-IRS4-AKT signaling axis, making itself as a promising druggable target for the disease.

The c-terminus of PI3K plays a key role in regulating kinase activity, with c-terminal disease-linked mutations leading to either activation or inhibition, which reveal a path to specific inhibitors.

Acute one-hour treatment of Pik3ca mutant mice with a novel anti-epilepsy drug suppresses seizures despite continued developmental brain dysmorphology, promising a new therapeutic strategy for patients with intractable pediatric epilepsy.

Single molecule reconstitution of PI3Kβ synergistic activation reveals mechanism for rapid PI(3,4,5)P₃ production during immune cell signaling.

Experimentation on patient biopsies, cell culture, and xenograft models demonstrates involvement of ErbB signaling and fibroblasts in lesion growth, implying that targeting of both stromal and endothelial cells could be a beneficial treatment strategy for patients with venous lesions.

Regulation of phosphoinositide 3 kinase (PI3Kγ) is essential in immune function, and stimuli that modulate the dynamics of the PI3Kγ helical domain can activate or inhibit kinase activity.

The p85α homodimer plays a role in the PI3K pathway by regulating PTEN function.

Inducible degradation of the insulin/insulin-like growth factor-1 receptor shows that a doubling in lifespan is possible even at extremely old ages in an organism.

Pathogenic activating mutations in PIK3CA or NRAS were the most common genetic findings in a lymphatic malformation patient cohort and an N-of-1 trial of the PI3Kα inhibitor alpelisib in a patient with a PIK3CA mutation confirmed these findings are actionable.