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 This evidence concerns the gene PRMT5 and cancer.