SMARCB1 and cancer: Initially, epigenetic therapies were found to be major drivers of retrotransposon reawakening.[102] This is mainly because epigenetic control mechanisms target endogenous retroviral elements to establish repressive heterochromatin.[103] Thus, it is not surprising that cancer‐associated mutations such as in H3.3,[104] SMARCB1[105] and DNMTA3A [106] can perturb the silencing of EREs and prime cancer cells for viral mimicry.