SOAT1 and neoplasm: However, distinct MTCL/L were identified to share genomic hallmarks and make use of the same pathways for their oncogenic drive [195], allowing the overarching development of targeted treatment approaches directed against tumor-specific molecular mechanisms; for example, genomic aberrations of members of the Janus(JAK)/signal transducer and activator of transcription (STAT) signaling, leading to constitutive activation of this pathway [196].