Finally, while no specific co‐occurring gene alteration was associated with a significant impact on OS in patients treated with ivosidenib, CDKN2A/B and MTAP alterations correlated with a worse PFS, suggesting a potential role in resistance to IDH1 inhibition or even the potential to combine IDH1 inhibitors with MTA‐cooperative PRMT5 inhibitors in MTAP deleted tumours to synergistically target different metabolic vulnerabilities. Here, IDH1 is linked to neoplasm.