On the individual-gene level in patient MBM, this finding seemed to be driven by upregulation of GFAP and HBB. Similar to our observation of upregulation of HBB in patient MBM samples, a multi-omic analysis of a large, multi-institutional melanoma cohort identified significant upregulation of HBB in addition to hemoglobin subunit alpha 1 mRNA levels in MBM compared to primary cutaneous melanomas [29]. This evidence concerns the gene HBB and melanoma.