Notably, caution is advised when interpreting the findings highlighted in this review, as a disrupted leptin/ObR axis may be either a consequence (e.g., secondary leptin-resistance due to hypothalamic lesion or obesity) or a promoter (local, systemic and exogenous leptin promotes tumor-genesis) of brain tumors, while both situations may show overlapping temporal dynamics [40]. The gene discussed is LEP; the disease is obesity disorder.