RICTOR and neoplasm: The molecular analysis showed a microsatellite-stable disease with low tumor mutation burden, and variable PTEN, PTCH1, KDM6A, ARv7, RB1, and PIK3CA loss/alteration, TP53 mutation, TMPRSS2-ERG fusion, and MYC, PIK3CB, RICTOR, or IRS2 amplification.