However, in 10%–15% TSC patients there is no pathogenic variant identified in either TSC1 or TSC2 genes based on standard clinical testing and are generally attributed to low mosaicism, deep intronic/promoter variants, and additional causative gene loci yet to be identified (Brook‐Carter et al., 1994; Curatolo et al., 2008; Klonowska et al., 2023; Sancak et al., 2005; Ye et al., 2022). This evidence concerns the gene TSC2 and tuberous sclerosis.