Abstract only Introduction: There is phenotypic and mechanistic overlap between arrhythmogenic right ventricular cardiomyopathy and cardiac sarcoidosis (CS). Whether CS and arrhythmogenic left ventricular cardiomyopathy (ALVC) similarly overlap has not been investigated. We aimed to evaluate the difference in proportions of disease-causing variants in ALVC-associated genes in patients with high clinical suspicion for CS. Methods: From a cohort of individuals with whole exome sequencing (WES) with linked electronic health record data in the Penn Medicine BioBank, we identified those who had and had not been referred for FDG-PET and cardiac MRI to evaluate for CS and compared demographics and carrier rates of predicted loss of function (pLOF) variants in genes causal for dilated cardiomyopathy (DCM) and ALVC. Results: Among 43,724 unrelated individuals with WES data, we identified 94 who had been referred for imaging to evaluate for CS. Those who had been referred for imaging were more often of self-reported Black race (50% vs. 25%, p<0.001) and had atrial arrhythmias (62% vs. 30%, p<0.001) and systolic heart failure (61% vs. 17%, p<0.001). Among these 94 individuals, six (6.4%) carried a pLOF variant in at least one of 19 genes known to have strong causal evidence for DCM/ALVC, compared with 1.2% of the participants not referred for imaging. After adjustment for age, sex, and five genetic principal components of ancestry, individuals referred for FDG-PET and MRI were more likely to carry a pLOF variant in a DCM gene of interest compared with the remaining PMBB participants (OR 5.96; 95% CI 2.31, 12.6; p<0.001). Conclusion: Individuals at high clinical suspicion for having CS have 6-fold higher odds of having a pLOF variant in a gene causal for DCM. There is under-recognized overlap between the clinical presentations of genetic ALVC/DCM and CS, and as such, the differential diagnosis for CS and inflammatory cardiomyopathy should be expanded to include these entities.