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The penetrance is incomplete and it is age and gender dependent. It is accepted as a disease of the sarcomere. Sixty percent of <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content> cases carry mutations in 1 of 8 sarcomere protein genes, mainly non\u2010sense <jats:styled-content style=\"fixed-case\">MYBPC3<\/jats:styled-content> and missense <jats:styled-content style=\"fixed-case\">MYH7<\/jats:styled-content> variants. Young patients with severe phenotype and other clinical features are included in proposed scores for prediction of high positive genetic result. The number of genes reported as disease\u2010causing has increased in the last few years, in some cases without robust evidence. Currently available in silico tools are not always useful for differentiation between benign and deleterious variants. There is enough information on genotype\u2010phenotype correlations to start understanding the mechanisms of the disease. Genetic and environmental modifiers have been explored with some interesting insights from <jats:styled-content style=\"fixed-case\">miRNA<\/jats:styled-content> studies with potential as biomarkers and therapeutic agents. There is an additional value of genetic testing in <jats:styled-content style=\"fixed-case\">HCM<\/jats:styled-content> for prognosis. 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