Aberrant assembly of SGs, PML bodies or paraspeckles may arise from dysregulation of or mutations in cancer-related proteins, thus promoting tumorigenesis. For instance, KRAS mutations promote SG hyper-assembly and this has been shown to confer a fitness advantage to cancer cells (Grabocka and Bar-Sagi, 2016). Likewise, mutations in DDX3X cause SG hyper-assembly and this has been shown to impair protein synthesis in medulloblastomas (Valentin-Vega et al., 2016). Moreover, YB-1 promotes SG assembly, which has been linked to increased invasion and metastasis (Somasekharan et al., 2015). The expression of PML/RARA leads to disruption of PML body assembly and deregulated transcriptional control of senescence and differentiation in acute promyelocytic leukemia (APL) (de Thé and Chen, 2010; Dos Santos et al., 2013). Furthermore, disruption of PML bodies contributes to APL pathogenesis by increasing genome instability (Voisset et al., 2018). Recombination-based alternative lengthening of telomeres (ALT) is a key mechanism for telomerase-negative cancer cells to maintain the telomere stability and the capability for unlimited proliferation (Bryan et al., 1997). ALT-associated PML bodies (APB) facilitate telomere maintenance and thus promote cancer cell immortality (Zhang et al., 2020). IL-6/STAT3 signaling promotes paraspeckles formation, which favors overactivation of STAT3 in human hepatocellular carcinoma (HCC) (Wang et al., 2018c). Paraspeckle assembly induced by p53 has been shown to inhibit cancer initiation in pancreatic cancer models (Mello et al., 2017). Finally, inhibition of amyloid body assembly has been shown to promote tumor tissue growth (Audas et al., 2016).