Genetic testing for the inherited risk of breast and ovarian cancer is well established but there has been considerable debate over which genes, beyond BRCA1 and BRCA2, genuinely belong in a clinical genetic testing panel. Following a period where many candidate genes have been proposed on minimal evidence and added to commercial testing panels, the last year has been characterised by the publication of several large data sets that provide a new scale of evidence to guide interpretation. This includes major international case-control studies (BRIDGES, CARRIERS), as well as local data (the BEACCON and BRA-STRAP studies). From this data a clearer picture of the true ‘moderate risk’ genes and their role in the Australian population, has emerged. The ‘new genes’ can be divided into two groups. Firstly, CHEK2 and ATM: genes associated particularly with an increased risk of estrogen receptor positive breast cancer, with relatively high frequency of pathogenic variants present in the population and potentially a wide range of other associated cancer risks. Secondly, the homologous recombination (HR) pathway genes RAD51C, RAD51D, BARD1, associated specifically with triple negative breast cancer and high grade serous ovarian cancer, very rare in the population but implicated in a classical ‘two-hit’ knock-out of the HR pathway that is central to the pathogenesis of these cancers. The new data has refined risk estimates in a number of areas of uncertainty, such as ovarian cancer risk for PALB2 – established as a moderate risk of ~5% lifetime cumulative incidence. It has also finally laid to rest claims for a significant role for a number of genes (such as RAD50, NBN, RECQL) that have been widely tested internationally, but should now be avoided in clinical practice.