Table 2.

Major developments in variable genes and host studies of H. pylori.

Genetics Studies	References
GC cells’ transition into a stemness stage and the regulating role of the Akt/FOXO3a axis.	[23]
For therapeutic intervention, CircPGD might be a promising new target.	[24]
One potential new target for GC therapy is lnc-PLCB1.	[25]
For stomach disorders linked to H. pylori, LINC00659 may prove to be a unique, promising prognostic and therapeutic marker.	[26]
H. pylori adhesion is decreased by the m6A alteration of the host LOX-1 mRNA.	[27]
One possible target for GC treatment could be USP35.	[28]
The proteins NCOR1, KIT, MITF, ESF1, ARNT2, TCF7L2, and KRR1 have been linked to GC, whether or not H. pylori is present.	[29]
An essential pathogenicity marker, the H. pylori oipA genotype, has been linked to the severity of gastric disorders.	[30]
Significance of baseline biopsies of the stomach antrum.	[31]
Api controls several GC hallmarks.	[32]
GAPDH has been identified as a heme chaperone.	[33]
SEA1 may be a potential treatment option.	[34]
Genetic variety of H. pylori in various parts of the world.	[35]
The development of GC and mortality related to H. pylori are linked to particular polymorphisms.	[36]
The TT genotype of rs7827435 and the CC genotype of rs10955176 may operate as protective factors against the risk of noncardia GC and H. pylori infection, respectively.	[37]
The course of an infection is determined by the interplay among virulence factors, phase-variable genes, and host genetics.	[38]