High‐risk neuroblastoma is broadly subdivided into two major cohorts: younger patients (toddlers) whose tumors show MYCN amplification, 1p deletion, and TERT overexpression; and older patients whose tumors harbor 11q deletion, occasionally along with other recurrent segmental chromosomal alterations (SCAs), maintain chromosome ends via the alternative lengthening of telomere mechanism, and generally show a slightly more inflamed TME [8, 9, 10, 11]. The gene discussed is MYCN; the disease is neuroblastoma.