In line with them, our comprehensive molecular analysis based on genomic analysis of three cases identified similar findings, mostly describing a microsatellite-stable disease with low tumor mutation burden, and variable PTEN, PTCH1, KDM6A, ARv7, and PIK3CA loss/alteration, TP53 mutation, TMPRSS2-ERG fusion, and MYC, PIK3CB, RICTOR, or IRS2 amplification. Here, PTCH1 is linked to neoplasm.