Whole genome sequencing (WGS) enables comprehensive molecular analysis of tumours and identification of hereditary cancer predisposition. According to the guidelines, directly determining pathogenic germline variants (PGVs) requires pre-test genetic counselling, which is cost-ineffective. Referral for genetic counselling based on tumour variants alone could miss relevant PGVs and/or result in unnecessary referrals. Here we sought to determine the optimal strategy with high PGV yield and a low number-needed-to counsel (NTC). Therefore, we compared the PGV yield and NTC of three simulated strategies, using paired tumour-normal WGS data from 937 metastatic patients. In strategy-1 genetic counselling of all 937 patients prior to the WGS-tumour testing allowed direct PGV analysis using a tumour type-specific gene panel. In strategy-2 and -3, germline testing and referral for post-test genetic counselling is based on tumour variants using adjusted Dutch guidelines (strategy-2) or ESMO-Precision Medicine Working Group recommendations (strategy-3). In strategy-1, clinically relevant PGVs would be detected in 50 patients (NTC=18.7). In strategy-2, 86 patients would have been referred for genetic counselling and 43 would have clinically relevant PGVs (NTC=2). In strategy-3, 94 patients would have been referred for genetic counselling and 32 would have clinically relevant PGVs (NTC=2.9). Hence, in strategy-2 and -3, 43 and 62 patients, respectively, were unnecessarily referred based on a somatic variant, primarily in BRCA1/2, PALB2, MLH1, and MSH2/6 genes. Both post-tumour test counselling strategies (2 and 3) had significantly lower NTC compared to pre-tumour test counselling (strategy-1). The adjusted Dutch guidelines had the highest PGV yield per NTC since it was also based on clinical criteria. Both post-tumour test counselling strategies could be improved by using a hybrid approach of directly analysing hereditary predisposition with counselling through mainstreaming for BRCA1/2, PALB2, MLH1, and MSH2/6 genes, along with tumour type-specific strategies for other cancer predisposition genes.