[5] The term "lineage-specific", since it relates to MITF, means genes or traits that are only found in a certain cell type.

Therefore, MITF may be involved in the rewiring of signaling cascades that are specifically required for the survival and physiological function of their normal cell precursors.

[9] The gene that encodes for MITF resides at the mi locus in mice,[10] and its protumorogenic targets include factors involved in cell death, DNA replication, repair, mitosis, microRNA production, membrane trafficking, mitochondrial metabolism, and much more.

In addition, current and future research can lead to potential avenues to target this transcription factor mechanism for cancer prevention.

The new MITF protein is unable to bind to DNA and melanocyte development and subsequently melanin production is altered.

A reduced number of melanocytes can lead to hearing loss, and decreased melanin production can account for the light skin and hair color that make Tietz syndrome so noticeable.

[13] Melanocytes are commonly known as cells that are responsible for producing the pigment melanin which gives coloration to the hair, skin, and nails.

Since it is a transcription factor that is involved in the regulation of genes related to invasiveness, migration, and metastasis, it can play a role in the progression of melanoma.

MITF recognizes E-box (CAYRTG) and M-box (TCAYRTG or CAYRTGA) sequences in the promoter regions of target genes.

Known target genes (confirmed by at least two independent sources) of this transcription factor include, Additional genes identified by a microarray study (which confirmed the above targets) include the following,[22] The LysRS-Ap4A-MITF signaling pathway was first discovered in mast cells, in which, the A mitogen-activated protein kinase (MAPK) pathway is activated upon allergen stimulation.

This complex consists of nine different aminoacyl-tRNA synthetases and three scaffold proteins and has been termed the "signalosome" due to its non-catalytic signalling functions.

The conformational change also switches LysRS activity from aminoacylation of Lysine tRNA to diadenosine tetraphosphate (Ap4A) production.

This mechanism is dependent on the precise length of the phosphate bridge in the Ap4A molecule so other nucleotides such as ATP or AMP will not affect it.

[43] MITF is also an integral part of melanocytes, where it regulates the expression of a number of proteins with melanogenic potential.

It has also been shown to be actively transported into the nucleus by directly interacting with the N-terminal domain of importin-β upon immunological stimulation of the mast cells.

[51][52][53] Serine phosphorylation is regulated by several signaling pathways including MAPK/BRAF/ERK, receptor tyrosine kinase KIT, GSK-3 and mTOR.

The Myc-associated zinc-finger protein related factor (MAZR) interacts with the Zip domain of MITF.

The combined loss of both genes results in severe osteopetrosis, pointing to an interaction between MITF and other members of its transcription factor family.

[64] The functional cooperation between MITF and the lymphoid enhancing factor (LEF-1) results in a synergistic transactivation of the dopachrome tautomerase gene promoter, which is an early melanoblast marker.

Although, the 5' UTR of MITF only consists of a nucleotide stretch of 123-nt, this region is predicted to fold into energetically favorable RNA secondary structures including multibranched loops and asymmetric bulges that is characteristics of IRES elements.