PARP-1 and its product PAR were found to be overexpressed in human colorectal cancer biopsies, and PARP-1 was shown to drive colorectal tumor progression in vivo.8 Very recently, a subset of colorectal cancers with deficiency in HR was identified, which displayed increased susceptibility to PARP inhibition, and at the same time, cross-sensitivity to oxaliplatin treatment.9 Furthermore, the MMR deficiency and the concomitant mutability induced by EGFR/BRAF inhibitor therapy likely promote neoantigen formation and immune cell activation, thus suggesting a combination with immunotherapy. Here, PARP1 is linked to hyperinsulinemic hypoglycemia, familial, 4.