SL‐based monoclonal antibody and targeted therapies support personalised cancer care through three main mechanisms: (i) precise targeting of defined genetic alterations, as exemplified by BRCA1/2 mutations; (ii) genotype‐guided regimen selection, such as combined PRMT5 and MAT2A inhibition in MTAP‐deleted gliomas to induce SL and enable genotype‐tailored regimens27; and (iii) overcoming acquired resistance, illustrated by regimens that combine ATR inhibitors (ATRis) with PARPis in the setting of resistance after PARPi monotherapy.28 The gene discussed is MAT2A; the disease is glioma.