Additionally, as previously mentioned, deletions involving the PI3K inhibitor PTEN are more prevalent in the GATA3-PTCL subtype of human PTCL-NOS than the TBX21-PTCL subtype [5], suggesting that the PI3K/AKT/mTOR enrichment frequently seen in tumors of this subtype may result from an increased susceptibility of this subtype to deletions in PTEN. This correlation seems similarly probable in canine CD4+ PTCL based on whole exome sequencing data identifying PTEN-mTOR pathway mutations in almost half of “Boxer type” canine T-cell lymphomas [46]. The gene discussed is MTOR; the disease is mature T-cell and NK-cell non-Hodgkin lymphoma.