MAK (male germ cell-associated kinase) is a serine/threonine protein kinase with critical roles in ciliary regulation and photoreceptor maintenance. Primary function: MAK regulates ciliary length and is essential for long-term photoreceptor survival through mechanisms involving cell cycle-dependent phosphorylation of FZR1 and transcriptional coactivation of androgen receptor (AR) 1. The protein localizes to multiple cellular compartments including centrosomes, the midbody, and photoreceptor inner segments, where it participates in intraciliary transport and cilium assembly. Mechanism: MAK exerts its effects through protein phosphorylation and intracellular signaling cascades, with evidence suggesting roles in chr6 stability and spermatogenesis, though detailed mechanistic pathways remain incompletely characterized. Disease relevance: MAK mutations cause autosomal recessive retinitis pigmentosa 62 (RP62), a progressive retinal degeneration. An Alu repeat insertion in MAK exon 9 causes loss of normal transcript and is enriched in Jewish populations, where it accounts for approximately one-third of recessive RP cases (1 in 55 carriers) 1. Clinical significance: Gene augmentation therapy shows promise; viral vector-mediated MAK restoration in patient-derived photoreceptor precursor cells and zebrafish models successfully restored ciliary length regulation and ameliorated visual defects without toxicity 1, supporting advancement toward clinical trials for MAK-associated RP treatment.