Contrariwise, tyrosine kinase activity of overexpressed EphA2 was also shown as required for the S897 phosphorylation via ERK to stimulate GBM cell prolifera-tion [112], thus showing the limit of a dichotomist view of canonical vs non-canonical EphA2 signaling and suggesting a more complex scenarios where both signaling modali-ties are highly interconnected [see also [28]]. Here, EPHA2 is linked to glioblastoma.