Given that resistance to erdafitinib in FGFR3-altered bladder cancer can arise through multiple mechanisms, such as increased P4HA2 expression, which stabilizes HIF-1α and reduces reactive oxygen species levels [40], FGFR3 gatekeeper mutations, TP53 alterations, and off-target resistance mechanisms including PI3K-mTOR activation and EGFR bypass signaling [41, 42], it is likely that similar diverse mechanisms contribute to erdafitinib resistance in FGFR1-driven bladder cancers. Here, MTOR is linked to urinary bladder cancer.