SOAT1 and neoplasm: Another research highlighted JAK-STAT pathway involvement in the relapsed samples; the authors performed WES on 14 matched primary/relapse samples from six DLBCL patients and recorded a mild increase of mutations in relapsed samples as compared to primary tumour specimens; 264 genes possibly related to therapy resistance were identified, such as tyrosine kinases, glycoproteins, and JAK-STAT pathway genes, as well as PIM1, SOCS1, and MYC, already known to be related to a risk for treatment failure [62].