We began our analysis on the LFS tumor cohort by investigating somatic driver mutations occurring in addition to TP53. Analysis of predicted driver mutations including SNVs, indels and structural variants (SVs) revealed several recurrently mutated genes and pathways including ATRX (n = 4), CTNNB1/APC (n = 4), homologous recombination (CHEK2, RAD51B, RAD51C) (n = 4) and PI3K/AKT signaling (PI3KCA, INPPL1, etc.)(n = 8). This evidence concerns the gene INPPL1 and neoplasm.