To assess whether ARID1A deficiency sensitizes bladder cancer cells to PI3K inhibitors, we performed dose-response cell viability experiments comparing ARID1Awt and ARID1Akd cell lines in the presence of alpelisib (a PI3K α-selective inhibitor), pictilisib (a PI3K pan-class I inhibitor), or dactolisib (a dual PI3K/mTOR inhibitor). This evidence concerns the gene ARID1A and urinary bladder carcinoma.