TMMs operate through two main pathways: the telomerase-dependent pathway, driven by upregulation of telomerase reverse transcriptase (TERT), which typically occurs via MYCN amplification (MNA) or rearrangements at the TERT locus; and the often-overlooked telomerase-independent pathway, represented in approximately 15 % of cancers [11,15,16], and notably, in more than 20 % of neuroblastomas [11,17], known as alternative lengthening of telomeres (ALT) [4]. This evidence concerns the gene TERT and neuroblastoma.