Fungicide resistance in powdery mildew and downy mildew of grapevines, caused by Erysiphe necator and Plasmopara viticola respectively, is an emerging issue in Australian vineyards (McKay et al., 2020). Between 2021 and 2025, samples of leaves and bunches with powdery and downy mildew symptoms were collected by growers and sent to the laboratory for fungicide resistance assessment using phenotyping (leaf disc assay) and genotyping (molecular detection of related mutations). A phenotypical sensitivity assay (Erickson & Wilcox, 1997, Savocchia et al., 2004) was used to assess nine and four fungicides for powdery and downy mildew, respectively. Genotypic analysis was conducted using two molecular techniques high-throughput qPCR (HT-qPCR, (Miles et al., 2021)) and high-throughput sequencing (HTS, (Sosnowski et al., 2023)). For powdery mildew, the presence of the G143A mutation in the cytochrome b gene (cytb), associated with the resistance to Quinone outside inhibitors (QoI, group 11), was investigated using HT-qPCR. The HTS was used to confirm the presence of G143A and investigate the presence of Y136F mutation in the cytochrome P450 eburicol 14α-demethylase (cyp51) gene, associated with resistance to Demethylation inhibitors (DMI, group 3) and H242x mutation in Succinate dehydrogenase (Sdh) gene, associated with resistance to Succinate dehydrogenase inhibitors (SDHI, group 7). For downy mildew, HTS was used to investigate the presence of G143A in the cytb gene and G1105S in the cellulose synthase (cesA3) gene associated with resistance to QoIs and Carboxylic acid amides (CAA group 40), respectively. Phenot1pic results showed that powdery mildew had reduced sensitivity to Amine (group 5) and SDHI fungicides and resistance to DMI, QoI and Aza-naphthalenes (group 13). Genotypic analysis showed that Y136F and G143A mutations were detected. However, the H242X mutant was not detected. Cross resistance has been detected for both aza-napthalenes (group 13 eg. proquinazid and quinoxyfen) and QoIs (group 11 eg. pyraclostrobin and azoxystrobin) in Australian samples but not for DMIs. Multisite resistance was identified in a number of samples for up to four fungicides (eg proquinazid, quinoxyfen, pyraclostrobin and azoxystrobin). Resistance was identified in downy mildew for QoI and phenylamides (PA, group 4), while reduced sensitivity was recorded for CAA. The G143A mutant was detected, but the G1105S mutation associated with CAA resistance was absent. Resistance in downy mildew was detected in growing regions where high disease pressure was present especially in the 2022/23 and 2023/24 seasons due to the above average rainfalls. The detection of phenotypical resistance of QoIs, in both powdery and downy mildew, was consistent with the detection of G143A mutation, suggesting that genotyping is sufficient for resistance detection for QoIs fungicides. However, the presence of Y136F, in powdery mildew, was not closely linked to the phenotypic resistance, suggesting other resistance mechanisms might be involved. Resistance management strategies, including rotation and withdrawing of the chemistries, are required to minimise and delay resistance to protect available fungicides. Continued and expanded monitoring crucial to managing and minimising fungicide resistance in Australia.