BackgroundThe solubilization of aluminum ions (Al3+) that results from soil acidity (pH < 5.5) is a limiting factor in oil palm yield. Al can be uptaken by the plant roots affecting DNA replication and cell division and triggering root morphological alterations, nutrient and water deprivation. In different oil palm-producing countries, oil palm is planted in acidic soils, representing a challenge for achieving high productivity. Several studies have reported the morphological, physiological, and biochemical oil palm mechanisms in response to Al-stress. However, the molecular mechanisms are just partially understood.ResultsDifferential gene expression and network analysis of four contrasting oil palm genotypes (IRHO 7001, CTR 3-0-12, CR 10-0-2, and CD 19 − 12) exposed to Al-stress helped to identify a set of genes and modules involved in oil palm early response to the metal. Networks including the ABA-independent transcription factors DREB1F and NAC and the calcium sensorCalmodulin-like(CML) that could induce the expression of internal detoxifying enzymes GRXC1, PER15, ROMT, ZSS1, BBI, and HS1 against Al-stress were identified. Also, some gene networks pinpoint the role of secondary metabolites like polyphenols, sesquiterpenoids, and antimicrobial components in reducing oxidative stress in oil palm seedlings. STOP1 expression could be the first step of the induction of common Al-response genes as an external detoxification mechanism mediated by ABA-dependent pathways.ConclusionsTwelve hub genes were validated in this study, supporting the reliability of the experimental design and network analysis. Differential expression analysis and systems biology approaches provide a better understanding of the molecular network mechanisms of the response to aluminum stress in oil palm roots. These findings settled a basis for further functional characterization of candidate genes associated with Al-stress in oil palm.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12870-023-04354-0.