Table 10. Verification of B entities from context-assignment based ABC model(FUS-TARDBP).

	B entity	Verifi- cation	Evidence
1	sod1	X	sod1 acts independently of fus and tardbp [49].
2	gli3	O	1) Fus is associated with ALS while, gli3 is associated with ALS through the shh pathway [50,51]. 2) Sonic hedgehog signaling in which gli3 participates and notch signaling can cooperate to regulate neurogenic divisions. Notch signaling may rescue tardbp [52,53].
3	c9orf72	O	1) Fus is associated with endosomal trafficking [54]. 2) Tardbp loss of function inhibits endosomal trafficking, c9orf72 regulates endosomal trafficking [55, 56].
4	vapb	O	1) Fus disrupts the vapb interactions to other signaling proteins [57]. 2) Mutations in vapb have already been shown to cause cytoplasmic transactive response tardbp accumulations [58].
5	mapt	O	1) Fus alternatively splices mapt [59]. 2) Tardbp is a component of ubiquitin-positive mapt-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis [60].
6	optn	O	ALS-linked cellular aggregates, include FUS, TDP-43(TARDBP), and OPTN [61]
7	grn	O	1) Grn affects tau phosphorylation [64]. 2) Grn mutations have abnormal accumulations of the TDP-43 protein in affected neurons [65].
8	taf15	O	TDP-43, FUS and TAF15 is associated with ALS and ALS-associated mutations identified in these genes are found in their C-terminal Gly-rich domains [66].