This mechanism is exemplified in Hodgkin’s lymphoma, where an ERV-derived LTR functions as an alternative promoter for the colony-stimulating factor 1 receptor (CSF1R) gene, driving its aberrant overexpression and subsequent activation of oncogenic signaling cascades such as PI3K/AKT and RAS/RAF/MEK/ERK pathways [123]. This evidence concerns the gene CSF1R and Hodgkins lymphoma.