For a study, researchers sought to understand that patients either had their tumors profiled using The Cancer Genome Atlas or had their tumors sequenced using the MSK-IMPACT clinical assay to screen for single-nucleotide variations, insertions and deletions, copy-number alterations, and structural rearrangements. Cox proportional-hazards regression models with a single variable and multiple variables were used to analyze the relationship between PIK3R1 alteration/expression and survival. For PIK3R1 siRNA-based knockdown-based functional analysis, they employed. A few prostate cancer patients from the MSK-IMPACT cohort underwent FDG-PET/CT scans using a hybrid positron emission tomography (PET)/CT scanner. Investigators found that metastatic malignancies had considerably more PIK3R1 mutations than initial cancers in their analysis of 1,417 human prostate tumors. In breast, gastric, and a number of other malignancies, including prostate cancer, PIK3R1 changes or lower mRNA expression were usually linked to worse clinical outcomes, particularly in the initial disease. PIK3R1 knockdown promoted cell proliferation and AKT activity in prostate cancer cell lines, particularly insulin-stimulated AKT activity. Loss or mutation of PIK3R1 was linked to increased susceptibility to AKT inhibitors in cell lines and organoids. The higher uptake of the glucose analog 18F-fluorodeoxyglucose by prostate tumors from PIK3R1-affected patients suggests enhanced glycolysis. According to their findings, the insulin-PIK3R1-glycolytic pathway in prostate cancer may be significantly regulated by PIK3R1 change, which also identifies a unique genetic trait of metastatic prostate cancer.