Cancer is fundamentally a genetic disease and heritable factors are amongst the most significant determinants of risk for many of the most common cancers as well as rare ‘syndromic tumours’. From the mid-1990’s mutations in individual genes have been found to explain Mendelian patterns of very high cancer risk – as with BRCA1, BRCA2 and the DNA mismatch repair genes. However these genes have provided explanations for only a small degree of the familial clustering of these cancers while many other tumour types remained unstudied and unexplained. The rapid development of genomic technologies in the last 5-10 years has opened new avenues to understanding familial risk. Hundreds of genome-wide association studies involving hundreds of thousands of patients internationally have delineated the contribution of common genomic variation to cancer risk, with the result that ‘polygenic risk’ has accounted for large proportions of the heritability for some tumour types. For the most successfully studied tumours such as prostate and breast cancer these studies have provided an explanation for almost half of the familial relative risk while the same approach has been less successful for other tumours (e.g. serous ovarian cancers), and the implications of this information for family members, compared to traditional high risk gene mutations, is only starting to be understood. Finally technologies such as whole exome or whole genome sequencing have now raised the possibility of identifying rare and unique genetic variants that were previously beyond reach and of combining these different domains of genetic risk into a complete picture of the inherited cancer risk for individuals and their families.